著者 廣畑 聡|
発行日 1997-03-25
出版物タイトル
資料タイプ 学位論文
JaLCDOI 10.18926/AMO/31831
フルテキストURL fulltext.pdf
著者 Hatipoglu, Omer Faruk| Hirohata, Satoshi| Yaykasli, Kursat Oguz| Cilek, Mehmet Zeynel| Demircan, Kadir| Shinohata, Ryoko| Yonezawa, Tomoko| Oohashi, Toshitaka| Kusachi, Shozo| Ninomiya, Yoshifumi|
抄録 <p>ADAMTS1 (a disintegrin and metalloproteinase with thrombospondin motifs 1) is an inflammatory-induced gene. We have previously reported that ADAMTS1 was strongly but transiently expressed in the infarcted heart. In this study, we investigated whether a 3'-untranslated region (UTR) affects the mRNA stability of this gene. When stimulated with tissue necrosis factor (TNF)-alpha, the expression level of ADAMTS1 mRNA rapidly increased, but the induction of ADAMTS1 mRNA peaked at 6h after stimulation, after which the expression levels of ADAMTS1 mRNA decreased. The 3'-UTR ADAMTS1 mRNA contains multiple adenine and uridine-rich elements, suggesting that the 3'-UTR may regulate gene stability. The addition of actinomycin D, an RNA synthesis inhibitor, demonstrated the decay of induced ADAMTS1 mRNA by TNF-alpha. Furthermore, a region containing multiple AUUUA motifs within the ADAMTS1 3'-UTR destabilized transfected Enhanced Green Fluorescence Protein (EGFP) mRNA expression. These results demonstrated that the ADAMTS1 3'-UTR may regulate the expression of ADAMTS1 mRNA.</p>
キーワード ADAMTS1 gene regulation metalloproteinase
Amo Type Original Article
発行日 2009-04
出版物タイトル Acta Medica Okayama
63巻
2号
出版者 Okayama University Medical School
開始ページ 79
終了ページ 85
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 19404339
Web of Sience KeyUT 000265457600002
著者 Demircan, Kadir| Hirohata, Satoshi| Nishida, Keiichiro| Hatipoglu, Omer F.| Oohashi, Toshitaka| Yonezawa, Tomoko| Apte, Suneel S.| Ninomiya, Yoshifumi|
発行日 2005-5
出版物タイトル Arthritis & Rheumatism
52巻
5号
資料タイプ 学術雑誌論文
著者 Toeda, Kenichi| Nakamura, Keigo| Hirohata, Satoshi| Hatipoglu, Omer F.| Demircan, Kadir| Yamawaki, Hitoshi| Ogawa, Hiroko| Kusachi, Shozo| Shiratori, Yasushi| Ninomiya, Yoshifumi|
発行日 2005-12
出版物タイトル Molecular and Cellular Biochemistry
280巻
1-2号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/53521
フルテキストURL 69_3_145.pdf
著者 Ishii, Hiroko| Kamikawa, Shigeshi| Hirohata, Satoshi| Mizutani, Akifumi| Abe, Koji| Seno, Masaharu| Oohashi, Toshitaka| Ninomiya, Yoshifumi|
抄録 Eosinophil cationic protein (ECP) is well known as a cationic protein contained in the basic granules of activated eosinophils. Recent studies have reported that ECP exhibits novel activities on various types of cells, including rat neonatal cardiomyocytes. Here we evaluated the effects of ECP on rat cardiac myoblast H9c2 cells. Our results showed that ECP enhanced the survival of the cells, in part by promoting the ERK and Akt/GSK-3β signaling pathways. ECP attenuated the cytotoxic effects of H2O2 on H9c2 cells as well as the production of reactive oxygen species, the number of apoptotic cells and caspase 3/7 activity in the cells. In conclusion, ECP activated the ERK and Akt/GSK-3β pathways, resulting in anti-oxidative effects on H9c2 cells that attenuated apoptosis.
キーワード ECP reactive oxygen species Akt ERK
Amo Type Original Article
発行日 2015-06
出版物タイトル Acta Medica Okayama
69巻
3号
出版者 Okayama University Medical School
開始ページ 145
終了ページ 153
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2015 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 26101190
Web of Sience KeyUT 000356903000003