PUTATIVE MECHANISM THROUGH WHICH N-CADHERIN-MEDIATED CELL CONTACT MAINTAINS CALCIUM HOMEOSTASIS AND THEREBY PREVENTS OVARIAN-CELLS FROM UNDERGOING APOPTOSIS
Jj. Peluso, PUTATIVE MECHANISM THROUGH WHICH N-CADHERIN-MEDIATED CELL CONTACT MAINTAINS CALCIUM HOMEOSTASIS AND THEREBY PREVENTS OVARIAN-CELLS FROM UNDERGOING APOPTOSIS, Biochemical pharmacology, 54(8), 1997, pp. 847-853
To date most of the studies involving the maintenance of ovarian cell
viability have focused on the endocrine, paracrine, and autocrine fact
ors that inhibit these cells from undergoing programmed cell death or
apoptosis. Recently, studies have demonstrated that cell contact also
prevents ovarian cells from dying via an apoptotic mechanism. In this
commentary, the role that hemophilic binding of the cell adhesion mole
cule, N-cadherin, plays in maintaining ovarian cell viability is prese
nted. These studies showed that N-cadherin hemophilic binding (1) is p
art of the mechanism through which cell contact maintains cell viabili
ty, (2) results in the activation (i.e. tyrosine phosphorylation) oi t
he fibroblast growth factor (FGF) receptor, and (3) prevents a sustain
ed elevation in intracellular free calcium ([Ca2+](i)) which triggers
apoptosis. These studies also revealed that hepatocyte growth factor (
HGF), also known as scatter factor (SF), disrupts cell contact, which
leads to a sustained increase in [Ca2+](i) levels and ultimately to ce
ll death. Based on these studies, this commentary presents a putative
mechanism that relates the cellular and molecular mechanism through wh
ich basic FGF, N-cadherin, and HGF/SF interact to regulate [Ca2+](i) l
evels and ultimately ovarian cell survival. (C) 1997 Elsevier Science
Inc.