{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T03:44:34Z","timestamp":1787802274553,"version":"build-2784847793"},"reference-count":55,"publisher":"The Endocrine Society","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:sec>\n                  <jats:title>Context:<\/jats:title>\n                  <jats:p>The initiation of term and preterm labor is associated with an up-regulated inflammatory response in myometrium; however, the underlying signaling pathways remain incompletely defined.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective:<\/jats:title>\n                  <jats:p>To define the regulatory mechanisms that mediate the increased myometrial inflammatory response leading to labor, we investigated the roles of microRNAs (miRNA\/miR).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design and Setting:<\/jats:title>\n                  <jats:p>Human myometrial tissues, isolated smooth muscle cells, and animal models were used to study miR-181a regulation of uterine inflammatory pathways and contractility.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Patients:<\/jats:title>\n                  <jats:p>Myometrial tissues from 15 term pregnant women undergoing elective cesarean section (not in labor) and 10 term pregnant women undergoing emergency cesarean section (in labor) were used.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results:<\/jats:title>\n                  <jats:p>Expression of the highly conserved microRNA, miR-181a, was significantly decreased in mouse and human myometrium during late gestation. By contrast, the putative miR-181a targets, TNF-\u03b1, and estrogen receptor (ER)-\u03b1, and the validated target, c-Fos, key factors in the inflammatory response leading to parturition, were coordinately up-regulated. In studies using human myometrial cells, overexpression of miR-181a mimics repressed basal as well as IL-1\u03b2-induced TNF-\u03b1, C-C motif chemokine ligand 2 and 8 expression, whereas the expression of the antiinflammatory cytokine, IL-10, was increased. Overexpression of miR-181a dramatically inhibited both spontaneous and IL-1\u03b2-induced contraction of human myometrial cells. Notably, miR-181a directly targeted ER\u03b1 and decreased its expression, whereas estradiol-17\u03b2 reciprocally inhibited expression of mature miR-181a in myometrial cells.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions:<\/jats:title>\n                  <jats:p>Thus, increased estradiol-17\u03b2\/ER\u03b1 signaling in myometrium near term inhibits miR-181a, resulting in a further increase in ER\u03b1 and proinflammatory signaling. This escalating feedback loop provides novel targets and therapeutic strategies for the prevention of preterm labor and its consequences.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/jc.2016-2078","type":"journal-article","created":{"date-parts":[[2016,7,26]],"date-time":"2016-07-26T17:05:38Z","timestamp":1469552738000},"page":"3646-3656","source":"Crossref","is-referenced-by-count":26,"title":["Reciprocal Feedback Between miR-181a and E2\/ER\u03b1 in Myometrium Enhances Inflammation Leading to Labor"],"prefix":"10.1210","volume":"101","author":[{"given":"Lu","family":"Gao","sequence":"first","affiliation":[{"name":"Department of Physiology (L.G., G.W., W.L.), Second Military Medical University, Shanghai 200433, People\u2019s Republic of China;"},{"name":"Department of Biochemistry (L.G., H.K., C.R.M.), University of Texas Southwestern Medical Center, Dallas, Texas 75390"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gang","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Physiology (L.G., G.W., W.L.), Second Military Medical University, Shanghai 200433, People\u2019s Republic of China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei-Na","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Physiology (L.G., G.W., W.L.), Second Military Medical University, Shanghai 200433, People\u2019s Republic of China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Holly","family":"Kinser","sequence":"additional","affiliation":[{"name":"Department of Biochemistry (L.G., H.K., C.R.M.), University of Texas Southwestern Medical Center, Dallas, Texas 75390"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hector L.","family":"Franco","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carole 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