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Submitted on May 27, 2003
Accepted on October 10, 2003
1 Prince Henry's Institute of Medical Research, P.O. Box 5152, Clayton, Victoria 3168, Australia
* To whom correspondence should be addressed. E-mail: chen.chen{at}phimr.monash.edu.au.
Available data on the influence of estradiol (E2) on growth hormone (GH) levels remains controversial. A factor contributing to this uncertainty is a lack of knowledge of both E2 action on somatotropes as well as the molecular mechanisms involved. In this study, we investigated gene expression implicated in GH secretion in somatotropes derived from female aromatase knockout (ArKO) mice. In these mice E2 production is blocked due to disruption of the Cyp19 gene encoding aromatase, the enzyme responsible for estrogen biosynthesis. The effect of E2 replacement was also studied by in vivo treatment of mice with E2 for 3 weeks. It was demonstrated that somatotropes from ArKO mice had a low expression of GH, GH-secretagogues receptor (GHS-R), GH-releasing hormone receptor (GHRH-R), and pituitary-specific transcription factor (Pit-1). On the other hand, the somatotropes exhibited elevated expression of somatostatin receptors (sstR1-5). Overall these effects resulted in a reduction in GH secretion. E2 replacement increased GHRH-R, Pit-1 and GH mRNA levels to 185%, 193% and 157%, and reduced the levels of sst1, sst2, sst4 and sst5 mRNA expression in ArKO mice respectively. E2 replacement did not affect the levels of pituitary estrogen (
and 
) and androgen receptor mRNA expression. It is concluded that expression of important genes involved in GH synthesis in somatotropes of the female ArKO mouse are functionally down-regulated and such a down-regulation is reversed to normal levels by E2 replacement. The levels of GHS-R, GHRH-R, and Pit-1 mRNA expression were also reduced, and sst1 and sst3 mRNA expression enhanced in aging ArKO and WT mice, resulting in a decrease of GH mRNA expression. It is suggested that aging is another important impact factor for the pituitary expression and regulation of GH mRNA in female mice.
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