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Department of Physiology Faculty of Medicine University of Manitoba Winnipeg, Manitoba, Canada R3E OW3
Address correspondence and requests for reprints to: Dr. L. J. Murphy, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3EOW3.
Abstract
The inability to convincingly demonstrate a mitogenic effect of estrogen on isolated uterine cells in culture suggests that autocrine or paracrine growth factors may be important in the estrogen-induced uterine proliferative response. Here we report that uterine expression of insulin-like growth factor-I (IGF-I), an important mediator of GH action, is increased after 17β-estradiol (5 µg/100 g bw, ip) administration to ovariectomized prepubertal rats. An increase in uterine IGF-I mRNA abundance, approximately 14-fold above untreated controls, was apparent 6 h after estrogen administration and the level achieved exceeded that seen in the uterus from intact mature rats during diestrus. In contrast to the increase in IGF-I expression in the uterus, no significant change in serum IGF-I concentration or hepatic or renal IGF-I mRNA abundance was demonstrable after 17β-estradiol injection of ovariectomized prepubertal rats. The increase in uterine IGF-I expression, was similar in both pituitary-intact and hypophysectomized, ovariectomized rats. We believe this is the first report of induction of IGF-I expression by estrogen in vivo. As such, the finding expands the role and significance of IGF-I as a mediator of growth beyond that related to GH.
FOOTNOTES
This work was supported by MRC Canada, the National Cancer Institute of Canada, and USPHS Grant HD-07843-13.
* Recipient of a C. J. Martin Travelling Fellowship from theNHMRC of Australia.
Recipient of an MRC Fellowship.
Received for publication March 18, 1987. Accepted for publication April 22, 1987.
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