{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T03:24:27Z","timestamp":1791170667552,"version":"4.1.0"},"reference-count":64,"publisher":"The Endocrine Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Although sex steroids have been implicated in the control of mammalian growth, their direct effect on GH synthesis is less clear. The aim of this study was to establish whether estradiol (E2) directly affects GH synthesis in somatotrophs. Somatotroph GH3 and MtT\/S cells were used as in vitro models. At physiological doses of E2 stimulation, GH mRNA levels were increased and the ER antagonist ICI 182,780 completely abolished this effect. Estrogen receptor (ER) \u03b1\u2013 and ER\u03b2-selective agonists, propylpyrazole triol (PPT), and 2,3-bis(4-hydroxyphenyl) propionitrile (DPN), respectively, augmented GH mRNA expression and secretion, whereas E2 and PPT, but not DPN increased prolactin (PRL) mRNA levels. E2, PPT, and DPN stimulated expression of the pituitary transcription factor Pou1f1 and increased its binding to the GH promoter. In vivo evidence of E2 effects on GH synthesis was obtained from the generation of the somatotroph-specific ER\u03b1 knockout (sER\u03b1-KO) mouse model. Basal pituitary GH, PRL, POU1F1, and ER\u03b1 mRNA expression levels were lower in sER\u03b1-KO mice compared with those in controls; whereas ER\u03b2 mRNA levels remained unchanged. E2 and DPN stimulated pituitary GH mRNA expression and serum GH levels in control and sER\u03b1-KO ovariectomized mice; however, serum GH levels were unchanged in PPT-treated ovariectomized sER\u03b1-KO mice. In these animal models, PRL mRNA levels increased after either E2 or PPT, but an increase was not seen after DPN treatment. Thus, we propose a mechanism by which estrogen directly regulates somatotroph GH synthesis at a pretranslational level. In contrast to the predominant effect of ER\u03b1 in the lactotroph, these results support a role for both ER\u03b1 and ER\u03b2 in the transcriptional control of Gh in the somatotroph and illustrate important differences in ER isoform specificity in the anterior pituitary gland.<\/jats:p>","DOI":"10.1210\/me.2013-1245","type":"journal-article","created":{"date-parts":[[2013,11,28]],"date-time":"2013-11-28T04:52:18Z","timestamp":1385614338000},"page":"40-52","source":"Crossref","is-referenced-by-count":61,"title":["Both Estrogen Receptor \u03b1 and \u03b2 Stimulate Pituitary GH Gene Expression"],"prefix":"10.1210","volume":"28","author":[{"given":"Dimiter","family":"Avtanski","sequence":"first","affiliation":[{"name":"Department of Pediatrics (D.A., H.J.N., S.W., C.J.R., S.R.), Johns Hopkins University School of Medicine, Baltimore, Maryland 21287"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Horacio J.","family":"Novaira","sequence":"first","affiliation":[{"name":"Department of Pediatrics (D.A., H.J.N., S.W., C.J.R., S.R.), Johns Hopkins University School of Medicine, Baltimore, Maryland 21287"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sheng","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Pediatrics (D.A., H.J.N., S.W., C.J.R., S.R.), Johns Hopkins University School of Medicine, Baltimore, Maryland 21287"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Romero","sequence":"first","affiliation":[{"name":"Department of Pediatrics (D.A., H.J.N., S.W., C.J.R., S.R.), Johns Hopkins University School of Medicine, Baltimore, Maryland 21287"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rhonda","family":"Kineman","sequence":"first","affiliation":[{"name":"Department of Pediatrics (D.A., H.J.N., S.W., C.J.R., S.R.), Johns Hopkins University School of Medicine, Baltimore, Maryland 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