{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T23:08:37Z","timestamp":1791328117375,"version":"4.3.1"},"reference-count":44,"publisher":"The Endocrine Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Stringent regulation of LH secretion from the pituitary is vital to ovarian function in mammals. Two rodent models of LH hypersecretion are the transgenic LH\u03b2-C-terminal peptide (LH\u03b2CTP) and estrogen receptor-\u03b1 (ER\u03b1)-null (\u03b1ERKO) mice. Both exhibit ovarian phenotypes of chronic anovulation, cystic and hemorrhagic follicles, lack of corpora lutea, interstitial\/stromal hyperplasia, and elevated plasma estradiol and testosterone. Because ER\u03b2 is highly expressed in granulosa cells of the ovary, we hypothesized the intraovarian actions of ER\u03b2 may be necessary for full manifestation of phenotypes associated with LH hyperstimulation. To address this question, we generated female mice that possess elevated LH, but lack ER\u03b2, by breeding the LH\u03b2CTP and ER\u03b2-null (\u03b2ERKO) mice. A comparison of LH\u03b2CTP, \u03b1ERKO, and \u03b2ERKOLHCTP females has allowed us to elucidate the contribution of each ER form to the pathologies and endocrinopathies that occur during chronic LH stimulation of the ovary. \u03b1ERKO ovaries respond to elevated LH by exhibiting an amplified steroidogenic pathway characteristic of the follicular stage of the ovarian cycle, whereas wild-typeLHCTP and \u03b2ERKOLHCTP females exhibit a steroidogenic profile more characteristic of the luteal stage. In addition, the hemorrhagic and cystic follicles of the LH\u03b2CTP and \u03b1ERKO ovaries require the intraovarian actions of ER\u03b2 for manifestation, because they were lacking in the \u03b2ERKOLHCTP ovary. In turn, ectopic expression of the Leydig cell-specific enzyme, Hsd17b3, and male-like testosterone synthesis in the \u03b1ERKO ovary are unique to this genotype and are therefore the culmination of elevated LH and the loss of functional ER\u03b1 within the ovary.<\/jats:p>","DOI":"10.1210\/en.2004-0548","type":"journal-article","created":{"date-parts":[[2004,7,2]],"date-time":"2004-07-02T00:28:14Z","timestamp":1088728094000},"page":"4693-4702","source":"Crossref","is-referenced-by-count":50,"title":["Formation of Cystic Ovarian Follicles Associated with Elevated Luteinizing Hormone Requires Estrogen Receptor-\u03b2"],"prefix":"10.1210","volume":"145","author":[{"given":"John F.","family":"Couse","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariana 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