γ-interferon inhibits rat granulosa cell differentiation in culture

A growing body of evidence indicates that factors secreted by cells of the immune system can directly affect a variety of endocrine phenomena. In the present study we examined the direct effects of the cytokine, interferon (IFN), on FSH-stimulated steroidogenesis and LH/hCG receptor induction in rat...

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Veröffentlicht in:	Biochemical and biophysical research communications 1988-12, Vol.157 (3), p.891-897
Hauptverfasser:	Gorospe, William C., Tuchel, Tammy, Kasson, Barry G.
Format:	Artikel
Sprache:	eng
Schlagworte:	20-alpha-Dihydroprogesterone - analogs & derivatives 20-alpha-Dihydroprogesterone - biosynthesis Analysis of the immune response. Humoral and cellular immunity Animals Biological and medical sciences Cell Differentiation Cells, Cultured Estrogens - biosynthesis Female Follicle Stimulating Hormone - pharmacology Fundamental and applied biological sciences. Psychology Fundamental immunology Granulosa Cells - cytology Granulosa Cells - drug effects Granulosa Cells - metabolism Immunobiology Interferon Type I - pharmacology Interferon-gamma - pharmacology Lymphokines, interleukins ( function, expression) Progesterone - biosynthesis Rats Receptors, LH - biosynthesis Receptors, LH - drug effects Regulatory factors and their cellular receptors
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Zusammenfassung:	A growing body of evidence indicates that factors secreted by cells of the immune system can directly affect a variety of endocrine phenomena. In the present study we examined the direct effects of the cytokine, interferon (IFN), on FSH-stimulated steroidogenesis and LH/hCG receptor induction in rat granulosa cells. We show that γ-IFN, but not α-IFN, inhibits FSH-stimulated progesterone, 20α-hydroxypregn-4-en-3-one and estrogen production as well as gonadotropin-induced LH/hCG receptor formation in a dose-dependent manner. The results suggest that γ-IFN may play a role in the maturation and differentiation of granulosa cells and thus may serve as a regulatory link between the immune and reproductive endocrine systems.
ISSN:	0006-291X 1090-2104
DOI:	10.1016/S0006-291X(88)80958-6