Follicular atresia and luteolysis. Evidence of a role for N-cadherin.

Details

Serval ID
serval:BIB_FEB61609B1EF
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Title
Follicular atresia and luteolysis. Evidence of a role for N-cadherin.
Journal
Annals of the New York Academy of Sciences
Author(s)
Makrigiannakis A., Coukos G., Blaschuk O., Coutifaris C.
ISSN
0077-8923 (Print)
ISSN-L
0077-8923
Publication state
Published
Issued date
2000
Volume
900
Pages
46-55
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; ReviewPublication Status: ppublish
Abstract
Studies suggest that cell-cell interactions may regulate apoptosis; and, in particular, the calcium-dependent cell adhesion molecule N-cadherin has been shown to be capable of modulating this process. Here, we review the evidence that N-cadherin is expressed by human granulosa cells (GCs) and mediates cell-cell adhesion between GCs. There is strong correlation between N-cadherin expression by granulosa or luteal cells and follicular survival in isolated follicles and archival tissue sections. There exists a strong expression of the molecule by GCs in follicles of the resting pool, of growing antral follicles, and of healthy corpora lutea. In contrast, the molecule is lost in degenerating GCs of atretic follicles and in luteal cells of the late luteal phase. Further, the experimental evidence demonstrates that cell-cell adhesion is critical to the survival of GCs and that N-cadherin-mediated cell-cell adhesion is a critical mediator of survival signals and inhibits apoptosis in these cells. Possible mechanisms by which apoptosis may be triggerred in GCs include the downregulation of N-cadherin, which is mediated, at least in part, through the enzymatic cleavage of the extracellular domain of the molecule. Collectively, these observations suggest that downregulation of N-cadherin or the absence of a functional extracellular domain of the molecule prevent GC aggregation and is associated with GC apoptosis. We propose that N-cadherin-mediated GC signaling plays a central role in follicular and luteal cell survival.
Keywords
Apoptosis/physiology, Cadherins/physiology, Cell Adhesion/physiology, Corpus Luteum/physiology, Female, Follicular Atresia/physiology, Humans
Pubmed
Web of science
Create date
14/10/2014 11:42
Last modification date
20/08/2019 16:29
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