EGF modulates phosphoinositide levels in ovarian granulosa cells stimulated by luteinizing hormone

Abstract

Hamster granulosa cells were exposed to epidermal growth factor (EGF) and luteinizing hormone (LH) to study cross-talk between second messenger pathways involving tyrosine kinase, cAMP, and phosphoinositides. Granulosa cells from ovarian preovulatory follicles of PMSG-primed hamsters were incubated with various additives in serum-free medium. LH, but not EGF, stimulated inositol phosphate (IP) accumulation; however, when combined with LH, EGF inhibited IP accumulation in a manner that was concentration dependent for both LH and EGF. The inhibitory effects of EGF were significantly reduced by the tyrosine kinase inhibitor genistein and by pertussis toxin suggesting a role for tyrosine kinase and an inhibitory G-protein (Gi) in this system. EGF stimulated an increase in cAMP, but it does not appear to modulate LH-stimulated IP levels via cAMP.

Mechanisms of vascular angiotensin II surface receptor regulation by epidermal growth factor

“…We considered the possibility that EGF dowregulates AngII surface receptor density through the production of cAMP, since cAMP has been shown to downregulate AngII receptors (Chen et al, 1994) and since EGF has been shown to promote the formation of cAMP (Ball et al, 1990; Budnik and Mukhopadhyay, 1991; Hubbard, 1994; Chen et al, 1995). To determine if cAMP downregulates AngII surface receptors in cultured VSMC, we incubated VSMC with stable cAMP analogues overnight and then determined AngII surface binding (Fig.…”

Pertussis toxin-sensitive G protein that supports vitellogenin uptake by promoting patency

“…That it supports yolk formation by suppressing cAMP levels in the follicle is suggested by two results: the effects of PTX on follicles, in particular the increases in Clexchange, K + uptake, and fluid uptake that result in the termination of epithelial patency, are also evoked by cell-permeant analogs of cAMP; and second, PTX-treatment resulted in a 34% increase in the cAMP content of follicles within 30 min. This degree of increase is also elicited by PTX in several mammalian cell lines (Bohm et al, 1994;Hubbard, 1994). The follicle is a multicompartmented system, however, and it is thus possible that the increase measured here is greater than 34% in the follicle cells, where PKA is mainly localized (Wang, 1996).…”

Pertussis toxin‐sensitive G‐proteins inhibit fibroblast growth factor‐induced signaling in pancreatic acini

“…Evidence for negative regulation of phospholipase C by G-proteins exists in a thyroid cell line FRTL5 and in ovarian granulosa cells (Bizzarri et al, 1990;Hubbard, 1994). In FRTL5 cells carbachol, a muscarinergic agonist, inhibits basal and norepinephrine-induced inosi-to1 phosphate generation in a pertussis toxin-sensitive fashion.…”