start-ver=1.4 cd-journal=joma no-vol=12 cd-vols= no-issue=1 article-no= start-page=17472 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20221027 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Neuromedin U-deficient rats do not lose body weight or food intake en-subtitle= kn-subtitle= en-abstract= kn-abstract=Studies in genetically modified mice establish that essential roles of endogenous neuromedin U (NMU) are anorexigenic function and metabolic regulation, indicating that NMU is expected to be a potential target for anti-obesity agents. However, in central administration experiments in rats, inconsistent results have been obtained, and the essential role of NMU energy metabolism in rats remain unclear. This study aims to elucidate the role of endogenous NMU in rats. We generated NMU knockout (KO) rats that unexpectedly showed no difference in body weight, adiposity, circulating metabolic markers, body temperature, locomotor activity, and food consumption in both normal and high fat chow feeding. Furthermore, unlike reported in mice, expressions of Nmu and NMU receptor type 2 (Nmur2) mRNA were hardly detectable in the rat hypothalamic nuclei regulating feeding and energy metabolism, including the arcuate nucleus and paraventricular nucleus, while Nmu was expressed in pars tuberalis and Nmur2 was expressed in the ependymal cell layer of the third ventricle. These results indicate that the species-specific expression pattern of Nmu and Nmur2 may allow NMU to have distinct functions across species, and that endogenous NMU does not function as an anorexigenic hormone in rats. en-copyright= kn-copyright= en-aut-name=YokogiKyoka en-aut-sei=Yokogi en-aut-mei=Kyoka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=GotoYuki en-aut-sei=Goto en-aut-mei=Yuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OtsukaMai en-aut-sei=Otsuka en-aut-mei=Mai kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OjimaFumiya en-aut-sei=Ojima en-aut-mei=Fumiya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=KobayashiTomoe en-aut-sei=Kobayashi en-aut-mei=Tomoe kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TsuchibaYukina en-aut-sei=Tsuchiba en-aut-mei=Yukina kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakeuchiYu en-aut-sei=Takeuchi en-aut-mei=Yu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NambaMasumi en-aut-sei=Namba en-aut-mei=Masumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KohnoMayumi en-aut-sei=Kohno en-aut-mei=Mayumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=TetsukaMinami en-aut-sei=Tetsuka en-aut-mei=Minami kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= en-aut-name=MatsuyamaMakoto en-aut-sei=Matsuyama en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=12 ORCID= en-aut-name=AizawaSayaka en-aut-sei=Aizawa en-aut-mei=Sayaka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=13 ORCID= affil-num=1 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=2 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=3 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=4 en-affil=Department of Natural Sciences and Biology, Kawasaki Medical School kn-affil= affil-num=5 en-affil=Division of Molecular Genetics, Shigei Medical Research Institute kn-affil= affil-num=6 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=7 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=8 en-affil=Division of Molecular Genetics, Shigei Medical Research Institute kn-affil= affil-num=9 en-affil=Division of Molecular Genetics, Shigei Medical Research Institute kn-affil= affil-num=10 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=11 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=12 en-affil=Division of Molecular Genetics, Shigei Medical Research Institute kn-affil= affil-num=13 en-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=375 cd-vols= no-issue=3 article-no= start-page=743 end-page=754 dt-received= dt-revised= dt-accepted= dt-pub-year=2018 dt-pub=20181030 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Runx3 regulates folliculogenesis and steroidogenesis in granulosa cells of immature mice en-subtitle= kn-subtitle= en-abstract= kn-abstract= We previously demonstrated that female Runx3 knockout (Runx3-/-) mice were anovulatory and their uteri were atrophic and that Runx3 mRNA was expressed in granulosa cells. To clarify how Runx3 regulates folliculogenesis and ovulation, we examine the effects of Runx3 knockout on the gene expression of growth factors associated with folliculogenesis and enzymes associated with steroidogenesis. In Runx3-/- mouse ovaries, the numbers of primary and antral follicles were lower than those in wild-type (wt) mice at 3 weeks of age, indicating that the loss of Runx3 affects folliculogenesis. The expression of genes encoding activin and inhibin subunits (Inha, Inhba and Inhbb) was also decreased in ovaries from the Runx3-/- mice compared with that in wt mice. Moreover, the expression of the genes Cyp11a1 and Cyp19a1 encoding steroidogenic enzymes was also decreased. In cultured granulosa cells from 3-week-old mouse ovaries, Cyp19a1 mRNA levels were lower in Runx3-/- mice than those in wt mice. Follicle-stimulating hormone (FSH) treatment increased Cyp19a1 mRNA levels in both wt and Runx3-/- granulosa cells in culture but the mRNA level in Runx3-/- granulosa cells was lower than that in wt ones, indicating that granulosa cells could not fully function in the absence of Runx3. At 3 weeks of age, gonadotropin α subunit, FSHβ subunit and luteinizing hormone (LH) β subunit mRNA levels were decreased in Runx3-/- mice. These findings suggest that Runx3 plays a key role in female reproduction by regulating folliculogenesis and steroidogenesis in granulosa cells. en-copyright= kn-copyright= en-aut-name=OjimaFumiya en-aut-sei=Ojima en-aut-mei=Fumiya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SaitoYuka en-aut-sei=Saito en-aut-mei=Yuka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TsuchiyaYukiko en-aut-sei=Tsuchiya en-aut-mei=Yukiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OgoshiMaho en-aut-sei=Ogoshi en-aut-mei=Maho kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FukamachiHiroshi en-aut-sei=Fukamachi en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=InagakiKenichi en-aut-sei=Inagaki en-aut-mei=Kenichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OtsukaFumio en-aut-sei=Otsuka en-aut-mei=Fumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Department of Biology, The Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=2 en-affil=Department of Biology, The Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=3 en-affil=Department of Biology, The Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=4 en-affil=Department of Biology, The Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=5 en-affil=The Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University kn-affil= affil-num=6 en-affil=The Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=7 en-affil=The Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=8 en-affil=Department of Biology, The Graduate School of Natural Science and Technology, Okayama University kn-affil= affil-num=9 en-affil=Department of Biology, The Graduate School of Natural Science and Technology, Okayama University kn-affil= en-keyword=Estrogen kn-keyword=Estrogen en-keyword=Follicle kn-keyword=Follicle en-keyword=Mouse kn-keyword=Mouse en-keyword=Ovary kn-keyword=Ovary en-keyword=Runx3 kn-keyword=Runx3 END start-ver=1.4 cd-journal=joma no-vol=33 cd-vols= no-issue= article-no= start-page=31 end-page=34 dt-received= dt-revised= dt-accepted= dt-pub-year=2017 dt-pub=201704 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Identification of Marker Gene of Pars Tuberalis Morphogenesis in Chicken Embryo. The expression of Cytokine-like 1 and Gap junction protein alpha 5 in the pars tuberalis kn-title=下垂体隆起部の発生期に特異的に発現する遺伝子Cytokine-like 1,Gap junction protein alpha 5の同定 en-subtitle= kn-subtitle= en-abstract= kn-abstract= Adenohypophysis delivered from oral ectoderm consists of pars distalis (PD), pars intermedia and pars tuberalis (PT). The mechanisms of development of PD has been well studied, and the cell differentiation of PD has been well understood. However, the morphogenesis and the differentiation of PT are still unclear, and the gene expression during the PT development remains largely unknown. In this study, we explored the specifically expressing genes in PT during development and analyzed its spatiotemporal expressions pattern. Microarray analysis on laser-captured PT and PD tissues obtained from chicken embryos on embryonic day 10 (E10.0) showed high expressing genes, Cytokine-like 1 (CYTL1) and Gap junction protein alpha 5 (GJA5) in PT. A detail analysis of spatiotemporal expressions pattern during chick embryo development by in situ hybridization revealed that CYTL1 mRNA was first detected in lateral head ectoderm and ventral head ectoderm in E1.5. The CYTL1 expressions moved into Rathke’s pouch at E2.5, then it was localized in PT primordium and continuously expressed in PT primordium until E12.0. On the other hand, GJA5 mRNA was transiently detected in PT primordium from E6 to E14.0, while the expression was not detected in PD during development. These results suggested that these genes may be involved in the regulation mechanism of PT development and could be a useful marker in the PT development. en-copyright= kn-copyright= en-aut-name=AizawaSayaka en-aut-sei=Aizawa en-aut-mei=Sayaka kn-aut-name=相澤清香 kn-aut-sei=相澤 kn-aut-mei=清香 aut-affil-num=1 ORCID= en-aut-name=HigakiYuriko en-aut-sei=Higaki en-aut-mei=Yuriko kn-aut-name=檜垣佑理子 kn-aut-sei=檜垣 kn-aut-mei=佑理子 aut-affil-num=2 ORCID= en-aut-name=OgoshiMaho en-aut-sei=Ogoshi en-aut-mei=Maho kn-aut-name=御輿真穂 kn-aut-sei=御輿 kn-aut-mei=真穂 aut-affil-num=3 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=4 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=5 ORCID= affil-num=1 en-affil=Graduate School of Natural Science and Technology, Okayama University kn-affil=岡山大学大学院自然科学研究科 affil-num=2 en-affil=Graduate School of Natural Science and Technology, Okayama University kn-affil=岡山大学大学院自然科学研究科 affil-num=3 en-affil=Graduate School of Natural Science and Technology, Okayama University kn-affil=岡山大学大学院自然科学研究科 affil-num=4 en-affil=Graduate School of Natural Science and Technology, Okayama University kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野 affil-num=5 en-affil=Graduate School of Natural Science and Technology, Okayama University kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野 END start-ver=1.4 cd-journal=joma no-vol=32 cd-vols= no-issue= article-no= start-page=19 end-page=21 dt-received= dt-revised= dt-accepted= dt-pub-year=2016 dt-pub=201604 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Structure and expression of quail PBCF gene kn-title=ウズラPBCF 遺伝子の構造と発現 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=KugimotoAyako en-aut-sei=Kugimoto en-aut-mei=Ayako kn-aut-name=釘本綾子 kn-aut-sei=釘本 kn-aut-mei=綾子 aut-affil-num=1 ORCID= en-aut-name=AizawaSayaka en-aut-sei=Aizawa en-aut-mei=Sayaka kn-aut-name=相澤清香 kn-aut-sei=相澤 kn-aut-mei=清香 aut-affil-num=2 ORCID= en-aut-name=OgoshiMaho en-aut-sei=Ogoshi en-aut-mei=Maho kn-aut-name=御輿真穂 kn-aut-sei=御輿 kn-aut-mei=真穂 aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=4 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=4 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=5 en-affil= kn-affil=岡山大学大学院自然科学研究科 END start-ver=1.4 cd-journal=joma no-vol=31 cd-vols= no-issue= article-no= start-page=37 end-page=39 dt-received= dt-revised= dt-accepted= dt-pub-year=2015 dt-pub=201504 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Analysis of Kallikrein expression in the mouse endometrium kn-title=マウス子宮内膜細胞におけるKallikrein の発現制御の解析 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TokumoriMegumi en-aut-sei=Tokumori en-aut-mei=Megumi kn-aut-name=徳森萌美 kn-aut-sei=徳森 kn-aut-mei=萌美 aut-affil-num=1 ORCID= en-aut-name=OgoshiMaho en-aut-sei=Ogoshi en-aut-mei=Maho kn-aut-name=御輿真穂 kn-aut-sei=御輿 kn-aut-mei=真穂 aut-affil-num=2 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=4 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ END start-ver=1.4 cd-journal=joma no-vol=30 cd-vols= no-issue= article-no= start-page=39 end-page=41 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=201404 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Breed difference in the regulation of feather coloration in chickens kn-title=ニワトリにおける羽色調節の品種差 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TakahashiToru en-aut-sei=Takahashi en-aut-mei=Toru kn-aut-name=高橋徹 kn-aut-sei=高橋 kn-aut-mei=徹 aut-affil-num=1 ORCID= en-aut-name=NishioKaori en-aut-sei=Nishio en-aut-mei=Kaori kn-aut-name=西尾香織 kn-aut-sei=西尾 kn-aut-mei=香織 aut-affil-num=2 ORCID= en-aut-name=OgoshiMaho en-aut-sei=Ogoshi en-aut-mei=Maho kn-aut-name=御輿真穂 kn-aut-sei=御輿 kn-aut-mei=真穂 aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=4 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=4 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=5 en-affil= kn-affil=岡山大学大学院自然科学研究科 END start-ver=1.4 cd-journal=joma no-vol=28 cd-vols= no-issue= article-no= start-page=40 end-page=43 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201204 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Microarray analysis sheds light on the molecular basis of sexual dichromatism in chickens kn-title=マイクロアレイによるニワトリ性的二色性の分子基盤の解析 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=FukaoAyaka en-aut-sei=Fukao en-aut-mei=Ayaka kn-aut-name=深尾彩加 kn-aut-sei=深尾 kn-aut-mei=彩加 aut-affil-num=1 ORCID= en-aut-name=NakaokaMinori en-aut-sei=Nakaoka en-aut-mei=Minori kn-aut-name=中岡実乃里 kn-aut-sei=中岡 kn-aut-mei=実乃里 aut-affil-num=2 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=3 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科 affil-num=4 en-affil= kn-affil=岡山大学大学院自然科学研究科 END start-ver=1.4 cd-journal=joma no-vol=22 cd-vols= no-issue=9 article-no= start-page=1011 end-page=1021 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=200509 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Organ-Specific and Age-Dependent Expression of Insulin-like Growth Factor-I (IGF-I) mRNA Variants: IGF-IA and IB mRNAs in the Mouse en-subtitle= kn-subtitle= en-abstract= kn-abstract=Insulin-like growth factor-I (IGF-I) gene generates several IGF-I mRNA variants by alternative splicing. Two promoters are present in mouse IGF-I gene. Each promoter encodes two IGF-I mRNA variants (IGF-IA and IGF-IB mRNAs). Variants differ by the presence (IGF-IB) or absence (IGF-IA) of a 52-bp insert in the E domain-coding region. Functional differences among IGF-I mRNAs, and regulatory mechanisms for alternative splicing of IGF-I mRNA are not yet known. We analyzed the expression of mouse IGF-IA and IGF-IB mRNAs using SYBR Green real-time RT-PCR. In the liver, IGF-I mRNA expression increased from 10 days of age to 45 days. In the uterus and ovary, IGF-I mRNA expression increased from 21 days of age, and then decreased at 45 days. In the kidney, IGF-I mRNA expression decreased from 10 days of age. IGF-IA mRNA levels were higher than IGF-IB mRNA levels in all organs examined. Estradiol-17 beta (E2) treatment in ovariectomized mice increased uterine IGF-IA and IGF-IB mRNA levels from 3 hr after injection, and highest levels for both mRNAs were detected at 6 hr, and relative increase was greater for IGF-IB mRNA than for IGF-IA mRNA. These results suggest that expression of IGF-I mRNA variants is regulated in organ-specific and age-dependent manners, and estrogen is involved in the change of IGF-I mRNA variant expression. en-copyright= kn-copyright= en-aut-name=OhtsukiTakashi en-aut-sei=Ohtsuki en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OtsukiMariko en-aut-sei=Otsuki en-aut-mei=Mariko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MurakamiYousuke en-aut-sei=Murakami en-aut-mei=Yousuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MaekawaTetsuya en-aut-sei=Maekawa en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=YamamotoTakashi en-aut-sei=Yamamoto en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=AkasakaKoji en-aut-sei=Akasaka en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=4 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=5 en-affil= kn-affil=Department of Mathematical and Life Science, Graduate School of Science, Hiroshima University affil-num=6 en-affil= kn-affil=Misaki Marine Biological Station, University of Tokyo affil-num=7 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=8 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University en-keyword=insulin like growth factor-I (IGF-I) kn-keyword=insulin like growth factor-I (IGF-I) en-keyword=uterus kn-keyword=uterus en-keyword=estradiol kn-keyword=estradiol en-keyword=mouse kn-keyword=mouse END start-ver=1.4 cd-journal=joma no-vol=22 cd-vols= no-issue=9 article-no= start-page=1003 end-page=1010 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=200509 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Interleukin-18 (IL-18) mRNA Expression and Localization of IL-18 mRNA-Expressing Cells in the Mouse Uterus en-subtitle= kn-subtitle= en-abstract= kn-abstract=Interleukin-18 (IL-18) belongs to the interleukin-1 family and was identified as an interferon gamma inducing factor. We investigated IL-18 mRNA-expressing cells in the mouse uterus. By RNase protection assay, IL-18 mRNA and a subunit of IL-18 receptor mRNA were detected in the uterus. In the uterus, IL-18 mRNA levels increased during sexual maturation. In situ hybridization analysis demonstrated IL-18 mRNA-expressing cells in the mouse uterus of different ages. At 21 days of age, IL-18 mRNA-expressing cells were detected in the luminal epithelial cells and stromal cells although the IL-18 mRNA signal was weak. At 42 days of age, IL-18 mRNA signal was mainly detected in the stromal cells located near the myometrium, and in some of the luminal and glandular epithelial cells. In the uterus of 63-day-old adult mice, a strong hybridization signal for IL-18 mRNA was detected at estrus, but was weak at diestrus. IL-18 mRNA was mainly detected in the glandular epithelial cells and stromal cells. The effect of estradiol-17 beta (E-2) on IL-18 mRNA-expressing cells in the uterus was examined in ovariectomized mice. In oil-treated mice IL-18 mRNA signal was localized in luminal epithelial cells and stromal cells, while in E-2-treated mice IL-18 mRNA signal was localized in stromal cells alone. These results suggest that the mouse uterus has an IL-18 system, and IL-18 exerts a physiological role within the uterus in a paracrine manner, and that IL-18 gene expression is regulated by estrogen. en-copyright= kn-copyright= en-aut-name=KusumotoKenji en-aut-sei=Kusumoto en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MurakamiYousuke en-aut-sei=Murakami en-aut-mei=Yousuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OtsukiMariko en-aut-sei=Otsuki en-aut-mei=Mariko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KanayamaMunetoshi en-aut-sei=Kanayama en-aut-mei=Munetoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=4 en-affil= kn-affil=Tsushima Facility, Advanced Science Research Center, Okayama University affil-num=5 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=6 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University en-keyword=interleukin-18 (IL-18) kn-keyword=interleukin-18 (IL-18) en-keyword=uterus kn-keyword=uterus en-keyword=estrogen kn-keyword=estrogen en-keyword=mouse kn-keyword=mouse END start-ver=1.4 cd-journal=joma no-vol=24 cd-vols= no-issue=3 article-no= start-page=241 end-page=247 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=200703 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Alternative Leader-Exon Usage in Mouse IGF-I mRNA Variants: Class 1 and Class 2 IGF-I mRNAs en-subtitle= kn-subtitle= en-abstract= kn-abstract=The mouse IGF-I gene contains six exons, and exon 1 and exon 2 gene are considered to be leader exons. The regulatory mechanism of alternative usage of the leader exons is unclear in mice. The present study, was aimed at clarifying changes in class 1 (derived from exon 1) and class 2 (derived from exon 2) IGF-I mRNA expression in mice under various conditions. Both class 1 and class 2 IGF-I mRNAs were expressed in the mouse uterus, liver and kidney, and class 1 IGF-I mRNA was the major transcript in all organs studied. In the uterus, both class 1 and class 2 IGF-I mRNA expression changed markedly during the estrous cycle, with the highest level at proestrus, but in the liver and kidney there were no significant changes in IGF-I mRNA expression during the estrous cycle. Estrogen treatment increased both class 1 and class 2 IGF-I mRNA levels in the uterus of ovariectomized mice, but class 1 mRNA expression increased more in response to estrogen treatment than class 2 mRNA expression. These findings suggest that estrogen stimulates IGF-I gene expression in, uterine cells, and that a promoter involved in transcription of class 1 IGF-I mRNA is more responsive to estrogen. In conclusion, the present study revealed that two leader exons of mouse IGF-I gene are used in the uterus, liver and kidney. IGF-I mRNA levels of both classes changed during the estrous cycle in the uterus, but not in the liver or kidney. Estrogen increased IGF-I mRNA levels of both classes in the uterus. en-copyright= kn-copyright= en-aut-name=OhtsukiTakashi en-aut-sei=Ohtsuki en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OtsukiMariko en-aut-sei=Otsuki en-aut-mei=Mariko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MurakamiYousuke en-aut-sei=Murakami en-aut-mei=Yousuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HirataKensaku en-aut-sei=Hirata en-aut-mei=Kensaku kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=4 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=5 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=6 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University en-keyword=IGF-I kn-keyword=IGF-I en-keyword=leader exon kn-keyword=leader exon en-keyword=estrogen kn-keyword=estrogen en-keyword=uterus kn-keyword=uterus en-keyword=mouse kn-keyword=mouse END start-ver=1.4 cd-journal=joma no-vol=26 cd-vols= no-issue=2 article-no= start-page=131 end-page=138 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200902 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Estradiol, Progesterone, and Transforming Growth Factor α Regulate Insulin-Like Growth Factor Binding Protein-3 (IGFBP3) Expression in Mouse Endometrial Cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=Insulin-like growth factor 1 (IGF1) Is Involved in the proliferation of mouse and rat endometrial cells in a paracrine or autocrine manner. Insulin-like growth factor binding protein-3 (IGFBP3) modulates actions of IGFs directly or indirectly. The present study aimed to determine whether IGFBP3 is Involved In the regulation of proliferation of mouse endometrial cells. Mouse endometrial epithelial cells and stromal cells were isolated, and cultured In a serum free medium. IGF1 stimulated DNA synthesis by endometrial epithelial and stromal cells, and IGFBP3 Inhibited IGF1-induced DNA synthesis. Estradiol-17 beta (E2) decreased the Igfbp3 mRNA level in endometrial stromal cells, whereas It Increased the Igf1 mRNA level. Transforming growth factor alpha (TGF alpha) significantly decreased IGFBP3 expression at both the mRNA and secreted protein levels in endometrial stromal cells. Progesterone (134) did not affect the E2-induced down-regulation of Igfbp3 mRNA expression in endometrial stromal cells, although P4 alone increased Igfbp3 mRNA levels. The present findings suggest that in mouse endometrial stromal cells E2 enhances IGF1 action through enhancement of IGF1 synthesis and reduction of IGFBP3 synthesis, and that TGF alpha affects IGF1 actions through modulation of IGFBP3 levels. en-copyright= kn-copyright= en-aut-name=MaekawaTetsuya en-aut-sei=Maekawa en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KanayamaMunetoshi en-aut-sei=Kanayama en-aut-mei=Munetoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University affil-num=4 en-affil= kn-affil=Department of Biology, Graduate School of Natural Science and Technology, Okayama University en-keyword=IGFBP3 kn-keyword=IGFBP3 en-keyword=IGF1 kn-keyword=IGF1 en-keyword=estrogen kn-keyword=estrogen en-keyword=mouse kn-keyword=mouse en-keyword=uterus kn-keyword=uterus END start-ver=1.4 cd-journal=joma no-vol=15 cd-vols= no-issue=4 article-no= start-page=573 end-page=579 dt-received= dt-revised= dt-accepted= dt-pub-year=1998 dt-pub=199808 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Insulin-Like Growth Factor-I and Its Receptor in Mouse Pituitary Glands en-subtitle= kn-subtitle= en-abstract= kn-abstract=Insulin-like growth factor-I (IGF-I) is produced in the liver and other peripheral tissues in response to growth hormone (GH) stimuli. IGF-I regulates diverse physiological functions in an autocrine and/or paracrine manner. IGF-I and IGF-I receptor (type-I receptor) are expressed in human and rat pituitary glands. However, the cell types of IGF-I-expressing cells and target cells of IGF-I in the pituitary glands are not known. The present study was aimed to identify the cell types of IGF-I-expressing cells and of its type-I receptor-expressing cells in mouse pituitary glands. In the mouse pituitary glands, IGF-I mRNA and IGF-I receptor mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). IGF-I-expressing cells and its receptor-expressing cells were detected by non-radioisotopic in situ hybridization using mouse IGF-I cDNA and IGF-I receptor cDNA probes, and their cell types were immunocytochemically determined using antibodies raised against pituitary hormones. We found that somatotrophs expressed both IGF-I and IGF-I receptors, and some of corticotrophs expressed IGF-I receptors. Co-localization of IGF-I and GH in the same cultured pituitary cells was observed by dual-labelling immunocytochemistry. The present study demonstrated that pituitary IGF-I produced in somatotrophs regulated functions of somatotrophs and corticotrophs in an autocrine and/or paracrine manner. en-copyright= kn-copyright= en-aut-name=HondaJunichi en-aut-sei=Honda en-aut-mei=Junichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FukumachiHiroshi en-aut-sei=Fukumachi en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biological Sciences, Graduate School of Science, University of Tokyo affil-num=4 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University END start-ver=1.4 cd-journal=joma no-vol=15 cd-vols= no-issue=4 article-no= start-page=567 end-page=572 dt-received= dt-revised= dt-accepted= dt-pub-year=1998 dt-pub=199808 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Augmentation of Prolactin Release by α-Melanocyte Stimulating Hormone Is Possibly Mediated by Melanocortin 3-Receptors in the Mouse Anterior Pituitary Cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=Suckling- and estrogen-induced prolactin release from the anterior pituitary is mediated by alpha-melanocyte stimulating hormone (a-MSH) secreted by the intermediate lobe of the pituitary in the rat. Melanocortin 5-receptors are expressed in the anterior pituitary and probably mediate the alpha-MSH function. In contrast, the mouse anterior pituitary does not express the receptor. To examine whether or not alpha-MSH regulates prolactin release in mice, we performed cell immunoblot assay using anterior pituitary cells from adult female mice. We found that alpha-MSH acted on mammotrophs (prolactin-secreting cells) and stimulated prolactin release in a dose dependent manner. A series of RT-PCR using oligonucleotide primer pairs specific for each subtypes of melanocortin receptors revealed that the melanocortin 3-receptor is the sole receptor expressed in the mouse anterior pituitary. These results suggest that alpha-MSH-induced prolactin release is mediated by melanocortin 3-receptors in female mice. en-copyright= kn-copyright= en-aut-name=MorookaYoshiaki en-aut-sei=Morooka en-aut-mei=Yoshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OomizuSouichi en-aut-sei=Oomizu en-aut-mei=Souichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=4 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University END start-ver=1.4 cd-journal=joma no-vol=17 cd-vols= no-issue=5 article-no= start-page=661 end-page=666 dt-received= dt-revised= dt-accepted= dt-pub-year=2000 dt-pub=200007 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Epidermal Growth Factor Stimulates Proliferation of Mouse Uterine Epithelial Cells in Primary Culture en-subtitle= kn-subtitle= en-abstract= kn-abstract=Epidermal growth factor (EGF) is one of growth factors that are thought to mediate the stimulatory effects of estrogen on the proliferation of uterine epithelial cells. The present study was attempted to obtain direct evidence for the mitogenic effects of EGF on uterine epithelial cells, and to prove that EGF and EGF receptors are expressed in these cells. Mouse uterine epithelial cells were isolated from immature female mice and cultured with or without EGF for 5 days. EGF (1 to 100 ng/ml) significantly increased the number of uterine epithelial cells, and the maximal growth (141.9+/-8.3% of controls) was obtained at a dose of 10 ng/ml. In addition, EGF (0.1 to 100 ng/ml) increased the number of DNA-synthesizing cells immunocytochemically detected by bromodeoxyuridine uptake to the nucleus. Northern blot analysis revealed that the uterine epithelial cells expressed both EGF mRNA (4.7 kb) and EGF receptor mRNAs (10.5, 6.6, and 2.7 kb) These results suggest that the proliferation of uterine epithelial cells is regulated by the paracrine and/ or autocrine action of EGF. Our previous study demonstrated the mitogenic effect of IGF-I on uterine epithelial cells. To examine whether the EGF- and IGF-I signaling act at the same level in the regulation of the proliferation of uterine epithelial cells, the cultured cells were simultaneously treated with IGF-I and EGF. IGF-I was found to additively stimulate the mitogenic effects of EGF, suggesting that the EGF-induced growth of uterine epithelial cells is distinct from IGF-l-induced growth. en-copyright= kn-copyright= en-aut-name=ShiragaMasahiro en-aut-sei=Shiraga en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KomatsuNoriko en-aut-sei=Komatsu en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TeshigawaraKiyoshi en-aut-sei=Teshigawara en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OkadaAkinobu en-aut-sei=Okada en-aut-mei=Akinobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=FukamachiHiroshi en-aut-sei=Fukamachi en-aut-mei=Hiroshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=4 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=5 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=6 en-affil= kn-affil=Department of Biological Sciences, Graduate School of Science, University of Tokyo affil-num=7 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University END start-ver=1.4 cd-journal=joma no-vol=19 cd-vols= no-issue=7 article-no= start-page=789 end-page=795 dt-received= dt-revised= dt-accepted= dt-pub-year=2002 dt-pub=200207 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Induction of mammotroph development by a combination of epidermal growth factor, insulin, and estradiol-17β in rat pituitary tumor GH3 cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=Several reports have indicated that prolactin-secreting cells (PRL cells) are generated from growth hormone-secreting cells (GH cells). We have shown that treatment with a combination of epidermal growth factor (EGF), insulin, and estradiol-17beta (E-2) induces the appearance of PRL cells in pituitary tumor GH3 cells. The aim of the present study was to clarify the involvement of mitosis in the cytogenesis of PRL cells in rat pituitary and GH3 cells. The effects of the treatment with EGF, insulin and E-2 on DNA-replication were studied by detecting the uptake of bromodeoxyuridine (BrdU) into the nucleus. In cultured rat pituitary cells, BrdU-labeled PRL cells were observed irrespective of the hormone treatment. In GH3 cells, BrdU-Iabeled GH cells and mammosomatotrophs (MS cells) were detected; BrdU-labeled PRL cells were not detected, however, when GH3 cells were treated with BrdU for 3 hr and then immediately examined for BrdU-labeling. BrdU-Iabeled PRL cells were found only when GH3 cells treated with BrdU were allowed to grow for another 3 days. This finding suggests that during the additional 3-day culture, BrdU-labeled PRL cells were generated from BrdU-Iabeled cells other than PRL cells. These results indicate that PRL cells are transdifferentiated from GH cells or VIS cells in GH3 cells by a combined treatment with EGF, insulin and E-2, while PRL cells in rat pituitaries are able to proliferate in response to the hormone treatment. Thus, there may be two pathways for cytogenesis of PRL cells the transdifferentiation of GH cells or VIS cells, and a self-duplication of PRL cells. en-copyright= kn-copyright= en-aut-name=KakeyaTomoshi en-aut-sei=Kakeya en-aut-mei=Tomoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University en-keyword=GH3 cells kn-keyword=GH3 cells en-keyword=pituitary kn-keyword=pituitary en-keyword=mammosomatotroph kn-keyword=mammosomatotroph en-keyword=mammotroph kn-keyword=mammotroph en-keyword=somatotroph kn-keyword=somatotroph END start-ver=1.4 cd-journal=joma no-vol=20 cd-vols= no-issue=1 article-no= start-page=83 end-page=89 dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=200301 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Gene Expression and the Physiological Role of Transforming Growth Factor-α in the Mouse Pituitary en-subtitle= kn-subtitle= en-abstract= kn-abstract=Transforming growth factor-alpha (TGF-alpha), a member of the epidermal growth factor (EGF) family, is produced within the mouse anterior pituitaries. However, the cell types of TGF-alpha-expressing cells and the physiological roles of TGF-a within mouse pituitary glands remain unclear. The aim of the present study was to localize TGF-alpha mRNA-expressing cells, and to clarify the involvement of TGF-alpha in estrogen-induced DNA replication in mouse anterior pituitary cells. Northern blot analysis demonstrated TGF-alpha mRNA expression in adult male and female mouse anterior pituitaries. In situ hybridization analysis of the pituitaries in these mice showed that TGF-alpha mRNA-expressing cells in the anterior pituitary are round, oval, and medium-sized. TGF-alpha mRNA was colocalized in most of the growth hormone (GH) mRNA-expressing cells, while only some of the prolactin (PRL) mRNA-expressing cells. DNA replication in the anterior pituitary cells was detected by monitoring the cellular uptake of a thymidine analogue, bromodeoxyuridine (BrdU) in a primary serum-free culture system. Estradiol-17beta (E2) and TGF-alpha treatment increased the number of BrdU-labelled mammotrophs, indicating that E2 and TGF-alpha treatment stimulates the DNA replication in mammotrophs. Immunoneutralization of TGF-alpha with anti-TGF-alpha-antibodies nullified the E2-induced increase in DNA replication. RT-PCR analysis of TGF-alpha mRNA expression in ovariectomized female mice revealed that E2 increases TGF-alpha mRNA levels. These results indicate that the TGF-alpha produced primarily in the somatotrophs mediates the stimulatory effects of estrogen on the DNA replication of pituitary cells in a paracrine or autocrine manner. en-copyright= kn-copyright= en-aut-name=SharmaSeema en-aut-sei=Sharma en-aut-mei=Seema kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OomizuSouichi en-aut-sei=Oomizu en-aut-mei=Souichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KakeyaTomoshi en-aut-sei=Kakeya en-aut-mei=Tomoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MasuiTohru en-aut-sei=Masui en-aut-mei=Tohru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=4 en-affil= kn-affil=National Institute of Health Sciences, Cell Bank affil-num=5 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=6 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University en-keyword=pituitary kn-keyword=pituitary en-keyword=transforming growth factor-α (TGF-α) kn-keyword=transforming growth factor-α (TGF-α) en-keyword=somatotroph kn-keyword=somatotroph en-keyword=mammotroph kn-keyword=mammotroph en-keyword=estrogen kn-keyword=estrogen END start-ver=1.4 cd-journal=joma no-vol=20 cd-vols= no-issue=5 article-no= start-page=639 end-page=645 dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=200305 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Epidermal Growth Factor and Transforming Growth Factor-α Stimulate the Proliferation of Mouse Uterine Stromal Cells en-subtitle= kn-subtitle= en-abstract= kn-abstract=Growth factors produced in the uterine endometrium are considered to be involved in the proliferation of the mouse uterine stromal cells induced by estradiol-17beta (E-2) and progesterone (P). The effect of epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha), one of EGF-related growth factors, on the proliferation of mouse uterine stromal cells was studied in a serum-free culture. The growth of the uterine stromal cells was measured by MTT assay. EGF was found to increase the number of uterine stromal cells in a dose-dependent manner. The DNA-replicating cells were investigated using the immunocytochemical detection of bromodeoxyuridine (BrdU)-labeled cells. EGF and TGF-alpha increased the percentage of BrdU-Iabeled cells in a dose-dependent manner. Administration of the combination of E-2 (10(-9) M) and P (10(-7) M) for 2 days increased the percentage of BrdU-Iabeled cells 2.3-fold. The stimulatory effect of EGF, TGF-a and the combination of E2 and P on DNA replication in the uterine stromal cells was repressed by RG-13022 (10(-5) M, the inhibitor of the EGF receptor tyrosine kinase). RT-PCR analysis of EGF-receptor-, TGF-alpha, and EGF-mRNA was carried,out in the cultured uterine stromal cells, and revealed the expression of those mRNAs. These data supported the hypothesis that uterine endometrial stromal growth induced by sex steroids required the EGF family of ligands such as EGF and TGF-alpha, both produced in the stromal cells, acting for DNA synthesis through EGF receptors. en-copyright= kn-copyright= en-aut-name=KomatsuNoriko en-aut-sei=Komatsu en-aut-mei=Noriko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MaekawaTetsuya en-aut-sei=Maekawa en-aut-mei=Tetsuya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=2 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=3 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University affil-num=4 en-affil= kn-affil=Department of Biology, Faculty of Science, Okayama University en-keyword=uterus kn-keyword=uterus en-keyword=endometrium kn-keyword=endometrium en-keyword=EGF kn-keyword=EGF en-keyword=TGF-α kn-keyword=TGF-α en-keyword=mouse kn-keyword=mouse END start-ver=1.4 cd-journal=joma no-vol=27 cd-vols= no-issue= article-no= start-page=31 end-page=35 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201105 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Physiological roles of Runx3 in female reproductive organs in mice kn-title=転写因子Pit-1の下垂体外組織における発現と下垂体ホルモンの発現制御 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TaniuchiShusuke en-aut-sei=Taniuchi en-aut-mei=Shusuke kn-aut-name=谷内秀輔 kn-aut-sei=谷内 kn-aut-mei=秀輔 aut-affil-num=1 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=2 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ END start-ver=1.4 cd-journal=joma no-vol=27 cd-vols= no-issue= article-no= start-page=26 end-page=30 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201105 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Physiological roles of Runx3 in female reproductive organs in mice kn-title=雌マウス生殖器官におけるRunx3の役割 en-subtitle= kn-subtitle= en-abstract= kn-abstract=Runx3(Runtdomaintranscriptionfactor3)はRunxファミリーに属する転写因子で雌マウスにおいてRunx3 mRNAは, 卵巣や子宮に発現していた。雌のRunx3(-/-)マウスは不妊であった。Runx3(-/-)マウスは卵胞形成異常を起こしており, 無排卵であった。一方で, 排卵能および黄体形成能は有していた。以上より, Runx3は卵胞形成および排卵制御に関与していることを明らかにした。Runx3(-/-)マウスの子宮は萎縮している。子宮内膜上皮細胞では, E2依存性の細胞増殖が起こらなかった。しかし,子宮内膜間質細胞では, E2, P4存在下で正常に細胞増殖が起きた。以上より, Runx3はE2による子宮の細胞増殖に関与していることを明らかにした｡ en-copyright= kn-copyright= en-aut-name=TsuchiyaYukiko en-aut-sei=Tsuchiya en-aut-mei=Yukiko kn-aut-name=土家由起子 kn-aut-sei=土家 kn-aut-mei=由起子 aut-affil-num=1 ORCID= en-aut-name=SakumaAtsuko en-aut-sei=Sakuma en-aut-mei=Atsuko kn-aut-name=佐久間敦子 kn-aut-sei=佐久間 kn-aut-mei=敦子 aut-affil-num=2 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=3 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ affil-num=4 en-affil= kn-affil=岡山大学大学院自然科学研究科生体統御学グループ END start-ver=1.4 cd-journal=joma no-vol=25 cd-vols= no-issue= article-no= start-page=3 end-page=6 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200903 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Intra-feather follicular melanocortin system regulates feather pigmentation in birds kn-title=黒色鶏やカラスはなぜ黒い? 〜下垂体中葉を欠く鳥類に体色制御のα-MSH調節系は存在するか〜 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科 END start-ver=1.4 cd-journal=joma no-vol=20 cd-vols= no-issue= article-no= start-page=36 end-page=39 dt-received= dt-revised= dt-accepted= dt-pub-year=2003 dt-pub=200309 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Physiological Roles of Pituitary Insulin-Like Growth Factor I -Intrapituitary Regulatory System- kn-title=下垂体インスリン様成長因子Tの生理的意義について―下垂体内制御機構について― en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=1 ORCID= en-aut-name=HondaJunichi en-aut-sei=Honda en-aut-mei=Junichi kn-aut-name=本多淳一 kn-aut-sei=本多 kn-aut-mei=淳一 aut-affil-num=2 ORCID= en-aut-name=ManabeYoshie en-aut-sei=Manabe en-aut-mei=Yoshie kn-aut-name=真鍋芳江 kn-aut-sei=真鍋 kn-aut-mei=芳江 aut-affil-num=3 ORCID= en-aut-name=MatsumuraRyusei en-aut-sei=Matsumura en-aut-mei=Ryusei kn-aut-name=松村龍成 kn-aut-sei=松村 kn-aut-mei=龍成 aut-affil-num=4 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 affil-num=2 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 affil-num=3 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 affil-num=4 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 affil-num=5 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 END start-ver=1.4 cd-journal=joma no-vol=21 cd-vols= no-issue= article-no= start-page=26 end-page=30 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200409 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=α-Melanocyte-Simulating Hormone Stimulates Prolactin Secretion kn-title=α-メラノサイト刺激ホルモンによるプロラクチン分泌の促進作用―下垂体中葉による前葉機能の制御機構― en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=1 ORCID= en-aut-name=MatsumuraRyusei en-aut-sei=Matsumura en-aut-mei=Ryusei kn-aut-name=松村龍成 kn-aut-sei=松村 kn-aut-mei=龍成 aut-affil-num=2 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 affil-num=2 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 affil-num=3 en-affil= kn-affil=岡山大学理学部生物学科生体制御科学講座 END start-ver=1.4 cd-journal=joma no-vol=22 cd-vols= no-issue= article-no= start-page=20 end-page=23 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=200512 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Expression of interleukin-18 gene in the mouse uterus kn-title=マウス子宮におけるインターロイキン-18遺伝子の発現 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MurakamiYousuke en-aut-sei=Murakami en-aut-mei=Yousuke kn-aut-name=村上要介 kn-aut-sei=村上 kn-aut-mei=要介 aut-affil-num=1 ORCID= en-aut-name=KusumotoKenji en-aut-sei=Kusumoto en-aut-mei=Kenji kn-aut-name=楠本憲司 kn-aut-sei=楠本 kn-aut-mei=憲司 aut-affil-num=2 ORCID= en-aut-name=OtsukiMariko en-aut-sei=Otsuki en-aut-mei=Mariko kn-aut-name=大月真理子 kn-aut-sei=大月 kn-aut-mei=真理子 aut-affil-num=3 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=4 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野 affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野 affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野 affil-num=4 en-affil= kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野 affil-num=5 en-affil= kn-affil=岡山大学大学院自然科学研究科高次生物科学講座･生体統御学分野 END start-ver=1.4 cd-journal=joma no-vol=24 cd-vols= no-issue= article-no= start-page=16 end-page=18 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=200712 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Effect of Blood Gas Value, Anesthesia Induction Time, and Arousal Time of the Mouse Under High and Reduced Pressures kn-title=マウス下垂体におけるプロオピオメラノコルチン遺伝子の発現制御 en-subtitle= kn-subtitle= en-abstract= kn-abstract=マウス下垂体前葉のACTH産生細胞では､CRH-R1を発現していた。POMC遺伝子プロモーターのTpit/PitxRE配列は､POMC遺伝子の転写活性を維持するのに重要であることを明らかにした。 en-copyright= kn-copyright= en-aut-name=MurakamiItsuo en-aut-sei=Murakami en-aut-mei=Itsuo kn-aut-name=村上逸雄 kn-aut-sei=村上 kn-aut-mei=逸雄 aut-affil-num=1 ORCID= en-aut-name=TakeuchiSakae en-aut-sei=Takeuchi en-aut-mei=Sakae kn-aut-name=竹内栄 kn-aut-sei=竹内 kn-aut-mei=栄 aut-affil-num=2 ORCID= en-aut-name=TakahashiSumio en-aut-sei=Takahashi en-aut-mei=Sumio kn-aut-name=高橋純夫 kn-aut-sei=高橋 kn-aut-mei=純夫 aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院自然科学研究科バイオサイエンス専攻 affil-num=2 en-affil= kn-affil=岡山大学大学院自然科学研究科バイオサイエンス専攻 affil-num=3 en-affil= kn-affil=岡山大学大学院自然科学研究科バイオサイエンス専攻 END