Document Detail

The Fas system is a key regulator of germ cell apoptosis in the testis.
MedLine Citation:
PMID:  9112408     Owner:  NLM     Status:  MEDLINE    
Apoptosis occurs in the testis as an important physiological mechanism to limit the number of germ cells in the seminiferous epithelium. Sertoli cells, which tightly regulate germ cell proliferation and differentiation, are implicated in the control of germ cell apoptosis. Fas (APO-1, CD95), a transmembrane receptor protein, transmits an apoptotic signal within cells when bound by Fas ligand (FasL). The Fas system has been implicated in immune regulation, including cytotoxic T cell-mediated cytotoxicity, activation-induced suicide of T cells, and control of immune-privileged sites. Here we propose the Fas system as a key regulator of spermatogenesis. In this model, FasL expressed by Sertoli cells initiates the apoptotic death of germ cells expressing Fas. Using immunohistochemistry, we localized Fas to germ cells and FasL to Sertoli cells. The expression of these genes was dramatically up-regulated after exposure to mono-(2-ethylhexyl) phthalate and 2,5-hexanedione, two widely studied Sertoli cell toxicants known to induce germ cell apoptosis. Mouse germ cells in vitro were susceptible to anti-Fas antibody-induced death, and the survival of rat germ cells was increased after disruption of FasL by antisense oligonucleotide treatment. Unlike its expression in other tissues, testicular expression of Fas in the lpr mouse, a spontaneous mutant of the Fas gene, is similar to that in the normal mouse, arguing for the importance of the Fas system in maintaining testicular homeostasis. These data implicate the Sertoli cell in the paracrine control of germ cell output during spermatogenesis by a Fas-mediated pathway.
J Lee; J H Richburg; S C Younkin; K Boekelheide
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Endocrinology     Volume:  138     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1997 May 
Date Detail:
Created Date:  1997-05-09     Completed Date:  1997-05-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2081-8     Citation Subset:  AIM; IM    
Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island 02912, USA.
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MeSH Terms
Antigens, CD95 / analysis,  metabolism*
Apoptosis / physiology*
Fas Ligand Protein
Gene Expression
Membrane Glycoproteins / analysis,  genetics,  physiology*
Mice, Inbred C57BL
RNA, Messenger / metabolism
Sertoli Cells / metabolism
Spermatogenesis / physiology
Spermatozoa / cytology*,  physiology
Testis / chemistry,  cytology*,  metabolism
Grant Support
Reg. No./Substance:
0/Antigens, CD95; 0/Fas Ligand Protein; 0/Fasl protein, mouse; 0/Membrane Glycoproteins; 0/RNA, Messenger; 0/Tnfsf6 protein, rat

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