Molecular Human Reproduction, Vol 3, 1095-1099, Copyright © 1997 by Oxford University Press
S Kol, I Ben-Shlomo, M Ando and EY Adashi
This study assessed the possibility that the intraovarian insulin-like
growth factor I (IGF-I) system interacts with the intraovarian
interleukin-1 (IL-1) system, the central role of which has been the subject
of increasing attention. To this end, whole ovarian dispersates from
immature rats were cultured for 48 h in the absence or presence of IGF-I or
IGF-binding protein-3 (IGFBP-3), with or without IL-1beta. Cellular RNA
content was subjected to a solution hybridization, RNase protection assay
with gel-purified [32P]-UTP-labelled antisense riboprobes for rat IL-1beta,
type I IL-1 receptor (IL-1R) and secretory phospholipase A2 (sPLA2). PLA2
activity in conditioned media was assayed by measuring the release of
[3H]-labelled palmitic acid from the sn-2 position of [3H]-labelled
phosphatidylcholine dipalmitoyl (PCDP) substrate. Treatment with IGF-I
resulted in a significant (P< 0.01) decrease in type I IL-1R transcripts
(an effect which was reversed by co-treatment with IL-1beta), was without
effect on IL-1beta transcripts, and significantly (P < 0.05) increased
sPLA2 gene expression (an effect which was further enhanced by co-treatment
with IL-1beta). Treatment with IGF-I resulted in a significant increase in
extracellular PLA2 activity over untreated control. These observations
suggest that IGF-I may down-regulate ovarian IL-1 action by decreasing type
I IL-1R gene expression, while up-regulating sPLA2 gene expression and
activity. These findings are consistent with a role for IGF-I in
suppressing IL-1 actions while promoting the generation of prostaglandins.
It is tempting to speculate that IGF-I, an intraovarian regulator concerned
with promoting folliculogenesis, may be also entwined with priming the
prostaglandin-producing potential in anticipation of subsequent ovulation.
JOURNAL ARTICLE
Insulin-like growth factor I affects the intraovarian interleukin-1 system: evidence for suppression of type I interleukin-1 receptor expression and enhancement of secretory phospholipase A2 expression and activity
Department of Obstetrics and Gynecology, University of Maryland School of Medicine, Baltimore 21201, USA.
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