Insulin-like growth factors as intraovarian regulators of granulosa cell growth and function.
A relatively large body of evidence now appears to support the existence of the essential ingredients for novel intraovarian IGF-driven control mechanisms. Indeed, evidence presented in this communication is in keeping with the possibility that the granulosa cell may be the site of IGF production, reception, and action. Although the relevance of IGFs to ovarian cell types other than the granulosa cell is largely unknown, one cannot at the present time exclude the possibility of nongranulosa cell contributions to intraovarian IGF production, reception, and action. Indeed, preliminary affinity cross-linking studies (Adashi, Resnick, Svoboda, Van Wyk and D'Ercole; unpublished data) suggest the existence of type-I and type-II receptors in nongranulosa cell compartments. The above notwithstanding, IGFs of granulosa (and possibly circulatory) origins may interact with granulosa cell autoreceptors either independently or in synergy with other granulosa cell agonists. According to this view, IGFs may act in the autocrine mode to stimulate granulosa cell replication on the one hand and promote granulosa cell differentiation on the other. Although proliferation and terminal differentiation may prove mutually exclusive under some circumstances, coexistence of the two processes is being increasingly recognized. In this context, some studies of porcine granulosa cells support a dual role for IGFs in granulosa cell ontogeny. As such, the IGFs can be added to a growing list of growth factors known to modulate granulosa cell growth and function, including EGF, PDGF, and FGF. Our findings indicate that Sm-C/IGF-I synergizes with FSH in the induction of rat granulosa cell aromatase activity at nanomolar concentrations compatible with its granulosa cell receptor binding affinity (thus far studied only in porcine cells. A role for Sm-C/IGF-I in the regulation of this key granulosa cell function would be in keeping with the possibility that Sm-C/IGF-I may partake in the assertion and maintenance of dominance by the selected follicle(s) or in promoting juvenile and early follicular development. Moreover, the ability of Sm-C/IGF-I to potentiate this and other FSH-driven ovarian functions may also account, at least in part, for the puberty-promoting effect of growth hormone. This permissive action of growth hormone has been initially suggested by observation in growth hormone-deficient rats, mice (dwarf mutants, and humans (sporadic, hereditary or acquired growth hormone deficiency.(ABSTRACT TRUNCATED AT 400 WORDS)
Adashi
E Y
EY
Resnick
C E
CE
D'Ercole
A J
AJ
Svoboda
M E
ME
Van Wyk
J J
JJ
D000818:Animals; D002454:Cell Differentiation; D002455:Cell Division; D005260:Female; D006107:Granulosa Cells / Q000166:cytology / Q000502:physiology*; D007328:Insulin / Q000502:physiology*; D007986:Luteinizing Hormone / Q000378:metabolism; D010053:Ovary / Q000166:cytology / Q000502:physiology*; D010455:Peptides / Q000502:physiology*; D011372:Progestins / Q000096:biosynthesis; D011509:Proteoglycans / Q000096:biosynthesis; D011956:Receptors, Cell Surface / Q000378:metabolism / Q000502:physiology; D011974:Receptors, LH; D017451:Receptors, Somatomedin; D013002:Somatomedins / Q000502:physiology*
D007328:Insulin; D010455:Peptides; D011372:Progestins; D011509:Proteoglycans; D011956:Receptors, Cell Surface; D011974:Receptors, LH; D017451:Receptors, Somatomedin; D013002:Somatomedins; D007986:Luteinizing Hormone