Androgen Receptor in Sertoli Cell Is Essential For Germ Cell Nursery and Junctional Complex Formation in Mouse Testes.

English | 正體中文 | 简体中文 | Items with full text/Total items : 45422/58598 (78%)
Visitors : 2517134 Online Users : 192

RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.

Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer

TMUIR > College of Medicine > Department of Medicine > Department of Obstetrics and Gynecology > Conference Paper > Item 987654321/16754

Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/16754

Title:	Androgen Receptor in Sertoli Cell Is Essential For Germ Cell Nursery and Junctional Complex Formation in Mouse Testes.
Authors:	曾啟瑞 Wang RS;Yeh SY;Chen LM;Lin HY;Zhang Caixia;Ni Jing;P;Anthony di Sant’Agnese;Karen L;deMe
Contributors:	醫學系婦產學科
Date:	2006
Issue Date:	2009-11-13 10:03:10 (UTC+8)
Abstract:	To examine the role of androgen receptor (AR) in Sertoli cells (SC), we used a SC-specific AR knockout (S-AR-/y) mouse to further evaluate the chronological changes of seminiferous tubules and the molecular mechanisms of SC androgen/AR signals on spermatogenesis. Testes morphology began changing as early as postnatal day (PD) 10.5 in wild-type (WT), but not in S-AR-/y mice. After puberty (PD 50), the SC nuclei of WT testes migrated to the basal area of the seminiferous epithelium; however, in S-AR-/y testes, SC nuclei were disarranged and dislocated. Results from electron microscopy further showed an obvious duplication of basal lamina of the seminiferous epithelium in S-AR-/y testes at PD 50 compared with WT testes. Using quantitative RT-PCR analyses, the expression of SC gene profiles were compared in PD 10.5 testes. In S-AR-/y testes, the expression levels of 1) vimentin were significantly increased and laminin alpha5 was significantly decreased in PD 10.5, which contributed to functional defects in cytoskeletons and production of the basement membrane component of SC leading to cell morphology deterioration and thus affecting the integrity of seminiferous epithelium; 2) claudin-11, occludin, and gelsolin were significantly decreased in PD 10.5, which contributed to defects in intact junctional complex formation of SC leading to impairment of the integrity of the blood-testis barrier; 3) calcium channel, voltage-dependent, P/Q-type, alpha1A subunit; tissue-type plasminogen activator; transferrin; and epidermal fatty-acid-binding protein were significantly decreased in PD 10.5, which contributed to functional defects in production and/or secretion of specific proteases, transport proteins, and paracrine factors of SC, leading to impairment of its germ cells' nursery functions.
Relation:	presented at Taiwan Society for Reproductive Medicine (TSRM) 2006 Annual Meeting, Taipei, Taiwan
Data Type:	conference
Appears in Collections:	[Department of Obstetrics and Gynecology] Conference Paper

Files in This Item:

File	Size	Format
H4-1.pdf	1822Kb	Adobe PDF	185	View/Open

著作權聲明 Copyright Notice

本平台之數位內容為臺北醫學大學所收錄之機構典藏，包含體系內各式學術著作及學術產出。秉持開放取用的精神，提供使用者進行資料檢索、下載與取用，惟仍請適度、合理地於合法範圍內使用本平台之內容，以尊重著作權人之權益。商業上之利用，請先取得著作權人之授權。
The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.
瀏覽或使用本平台，視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例，並不得為任何不法目的使用TMUIR。
By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.
本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者，煩請權利人通知本平台維護人員([email protected])，將立即採取移除該數位著作等補救措施。
TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

Loading...