{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T11:43:41Z","timestamp":1791546221021,"version":"4.3.4"},"reference-count":59,"publisher":"The Endocrine Society","issue":"2","license":[{"start":{"date-parts":[[2020,11,28]],"date-time":"2020-11-28T00:00:00Z","timestamp":1606521600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,1,23]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Enhanced levels of catecholestradiols, 2-hydroxyestradiol (2-OHE2) or 4-hydroxyestradiol (4-OHE2), are reported in endometriosis. During gestation, catecholestradiol activation of adrenergic receptors (AR) elevates estrogen receptor (ER)-independent proliferation of uterine arterial endothelial cells.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>To investigate \u03b2-AR-mediated catecholestradiol effects on human endometrial stromal cell (HESC) and epithelial cell survival in endometriosis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>\u03b2-AR immunostaining of eutopic and ectopic endometria (n\u2005=\u20059). Assays for cell viability, 5-bromo-2\u2032-deoxyuridine proliferation, apoptosis, quantitative PCR, and estrogenicity (alkaline phosphatase activity), as well as siRNA \u03b2-AR silencing and immunoblot analyses of cultured HESCs or Ishikawa cells treated with control or 2-OHE2 or 4-OHE2 \u00b1\u03b2-AR antagonist or \u00b1p38 MAPK inhibitor.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Setting<\/jats:title>\n                  <jats:p>University research institution.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Patients<\/jats:title>\n                  <jats:p>Women with or without endometriosis.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Interventions<\/jats:title>\n                  <jats:p>None.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Main Outcome Measures<\/jats:title>\n                  <jats:p>\u03b2-AR expression in eutopic vs ectopic endometria and regulation of HESC survival by 2-OHE2 and 4-OHE2.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Eutopic and ectopic endometrial stromal and epithelial cells displayed \u03b22-AR immunoreactivity with increased staining in the functionalis vs basalis layer (P\u2005&amp;lt;\u20050.05). Both 2-OHE2 and 4-OHE2 enhanced HESC and Ishikawa cell survival (P\u2005&amp;lt;\u20050.05), an effect abrogated by \u03b2-AR antagonist propranolol, but not ER antagonist ICI182,780. 2-OHE2 or 4-OHE2 failed to induce cell survival and estrogenic activity in ADRB2-silenced HESCs and in Ishikawa cells, respectively. Although 2-OHE2 inhibited apoptosis and BAX mRNA expression, 4-OHE2 induced proliferation and decreased apoptosis (P\u2005&amp;lt;\u20050.05). Both catecholestradiols elevated phospho-p38 MAPK levels (P\u2005&amp;lt;\u20050.05), which was blocked by propranolol, and p38 MAPK inhibitor reversed catecholestradiol-enhanced HESC survival.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Catecholestradiols increase endometrial cell survival by an ER-independent \u03b2-AR-mediated p38 MAPK activation, suggesting that agents blocking \u03b2-AR (e.g., propranolol) or inhibiting 2-OHE2- or 4-OHE2-generating enzymes (i.e., CYP1A1\/B1) could treat endometriosis.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgaa866","type":"journal-article","created":{"date-parts":[[2020,11,28]],"date-time":"2020-11-28T12:46:46Z","timestamp":1606567606000},"page":"337-350","source":"Crossref","is-referenced-by-count":12,"title":["Catecholestradiol Activation of Adrenergic Receptors Induces Endometrial Cell Survival via p38 MAPK Signaling"],"prefix":"10.1210","volume":"106","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1003-1631","authenticated-orcid":false,"given":"Rachel","family":"Sprague","sequence":"first","affiliation":[{"name":"Department of Obstetrics & Gynecology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joung W","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Obstetrics & Gynecology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Esma","family":"Kirimlioglu","sequence":"additional","affiliation":[{"name":"Department of Obstetrics & Gynecology, Morsani College of Medicine, University of South Florida, Tampa, FL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaofang","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Obstetrics & 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