Epidermal growth factor receptor binding and biological activity in
the ovary of goldfish, carassius auratus.
Pati, Debananda, Kerry Balshaw, Daniel L. Grinwich, Morley D.
Hollenberg, and Hamid R. Habibi.
Endocrine Research Group, Department of Biological Sciences and
Department of of Pharmacology & Therapeutics, University of
Calgary, Calgary, Alberta, Canada T2N 1N4
APStracts 2:0328R, 1995.
The receptor binding and biological activity of epidermal growth
factor-urogastrone (EGF) was characterized in the follicle-enclosed
goldfish oocyte. The binding of 125I-mouse EGF (mEGF) to goldfish
ovarian membrane preparation was peptide-specific, saturable,
reversible and dependent on time and tissue concentration. Binding
data analysis indicated the presence of a single class of high
affinity binding sites with an estimated equilibrium dissociation
constant (Kd) of 4.4 +/- 1.8 x 10-10 M. The 125I-mEGF binding was
displaced by unlabeled mEGF and by human recombinant transforming
growth factor alpha (hTGF-[alpha]). Both mEGF and hTGF-[alpha] were
found to stimulate reinitiation of oocyte meiosis as indicated by
germinal vesicle breakdown (GVBD). Treatment with mEGF and hTGF
-[alpha] stimulated GVBD from a basal level of 8.5% to approximately
30% with estimated ED50 values for EGF of 5.80 +/- 0.82 x 10-10 and
for hTGF-[alpha], 1.9 +/- 1.0 x 10-10 M. Furthermore, treatment with
mEGF marginally increased 17[alpha],20[beta]-dihydroxy-4-pregnen-3
-one (DHP)-induced GVBD, without significantly influencing the
gonadotropin-induced response. Treatment with either mEGF or hTGF
-[alpha] significantly reduced human chorionic gonadotropin (HCG)
-stimulated testosterone production in a concentration-related manner.
These data suggest that members of the EGF family may play a role in
the regulation of ovarian function in goldfish.
Received 10 May 1995; accepted in final form 13 November 1995.
APS Manuscript Number R279-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95