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ID 67470
フルテキストURL
fulltext.pdf 16.6 MB
著者
Ikeda, Shiori Department of Cytology and Histology, Medical School, Okayama University
Sato, Keita Department of Cytology and Histology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University ORCID Kaken ID publons researchmap
Fujita, Hirofumi Department of Cytology and Histology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Kaken ID publons researchmap
Ono-Minagi, Hitomi Department of Cytology and Histology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Miyaishi, Satoru Department of Legal Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Kaken ID publons researchmap
Nohno, Tsutomu Department of Cytology and Histology, Medical School, Okayama University
Ohuchi, Hideyo Department of Cytology and Histology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University ORCID Kaken ID researchmap
抄録
The mouse Harderian gland (HG) is a secretory gland that covers the posterior portion of the eyeball, opening at the base of the nictitating membrane. The HG serves to protect the eye surface from infection with its secretions. Mice open their eyelids at about 2 weeks of age, and the development of the HG primordium mechanically opens the eye by pushing the eyeball from its rear. Therefore, when HG formation is disturbed, the eye exhibits enophthalmos (the slit-eye phenotype), and a line of Fgf10(+/-) heterozygous loss-of-function mice exhibits slit-eye due to the HG atrophy. However, it has not been clarified how and when HGs degenerate and atrophy in Fgf10(+/-) mice. In this study, we observed the HGs in embryonic (E13.5 to E19), postnatal (P0.5 to P18) and 74-week-old Fgf10(+/-) mice. We found that more than half of the Fgf10(+/-) mice had markedly degenerated HGs, often unilaterally. The degenerated HG tissue had a melanized appearance and was replaced by connective tissue, which was observed by P10. The development of HGs was delayed or disrupted in the similar proportion of Fgf10(+/-) embryos, as revealed via histology and the loss of HG-marker expression. In situ hybridization showed Fgf10 expression was observed in the Harderian mesenchyme in wild-type as well as in the HG-lacking heterozygote at E19. These results show that the Fgf10 haploinsufficiency causes delayed or defective HG development, often unilaterally from the unexpectedly early neonatal period.
キーワード
Harderian gland
Fgf10
haploinsufficiency
mouse
発行日
2024-06-03
出版物タイトル
Journal of Developmental Biology
12巻
2号
出版者
MDPI
開始ページ
16
ISSN
2221-3759
資料タイプ
学術雑誌論文
言語
英語
OAI-PMH Set
岡山大学
著作権者
© 2024 by the authors.
論文のバージョン
publisher
PubMed ID
DOI
Web of Science KeyUT
関連URL
isVersionOf https://doi.org/10.3390/jdb12020016
ライセンス
https://creativecommons.org/licenses/by/4.0/
Citation
Ikeda, S.; Sato, K.; Fujita, H.; Ono-Minagi, H.; Miyaishi, S.; Nohno, T.; Ohuchi, H. Harderian Gland Development and Degeneration in the Fgf10-Deficient Heterozygous Mouse. J. Dev. Biol. 2024, 12, 16. https://doi.org/10.3390/jdb12020016
助成機関名
Japan Society for the Promotion of Science
助成番号
JP20K21655
JP20K08885
JP23K05850
JP24K09998