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Estrogen receptor (ER) \u03b2 may play a role in regulating this process.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Intestinal tissue samples from stenotic and nonstenotic regions were collected from Crohn\u2019s disease (CD) patients. RNA sequencing was conducted on a mouse model to identify differentially expressed mRNAs. Histological, immunohistochemical, and semiquantitative Western blotting analyses were employed to assess ECM deposition and fibrosis. The roles of relevant pathways in fibroblast transdifferentiation, activity, and migration were examined.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Estrogen receptor \u03b2 expression was found to be downregulated in the stenotic intestinal tissue of CD patients. Histological fibrosis score, collagen deposition, and profibrotic molecules in the colon of an intestinal fibrosis mouse model were significantly decreased after activation of ER\u03b2. In vitro, ER\u03b2 activation alleviated transforming growth factor (TGF)-\u03b2-induced fibroblast activation and migration, as evidenced by the inhibition of col1\u03b11, fibronectin, \u03b1-smooth muscle actin (\u03b1-SMA), collagen I, and N-cadherin expression. RNA sequencing showed that ER\u03b2 activation affected the expression of genes involved in ECM homeostasis and tissue remodeling. Enrichment analysis of differentially expressed genes highlighted that the downregulated genes were enriched in ECM-receptor interaction, TGF-\u03b2 signaling, and Toll-like receptor (TLR) signaling. Western blotting confirmed the involvement of TGF-\u03b2\/Smad and TLR4\/MyD88\/NF-\u03baB signaling pathways in modulating fibrosis both in vivo and in vitro. The promoter activity of TGF-\u03b21 and TLR4 could be suppressed by ER\u03b2 transcription factor.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Estrogen receptor \u03b2 may regulate intestinal fibrosis through modulation of the TGF-\u03b2\/Smad and TLR4\/MyD88\/NF-\u03baB signaling pathways. Targeting ER\u03b2 activation could be a promising therapeutic strategy for treating intestinal fibrosis.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ibd\/izae156","type":"journal-article","created":{"date-parts":[[2024,7,31]],"date-time":"2024-07-31T01:08:42Z","timestamp":1722388122000},"page":"11-27","source":"Crossref","is-referenced-by-count":16,"title":["Estrogen Receptor \u03b2 Activation Mitigates Colitis-associated Intestinal Fibrosis via Inhibition of TGF-\u03b2\/Smad and TLR4\/MyD88\/NF-\u03baB Signaling Pathways"],"prefix":"10.1093","volume":"31","author":[{"given":"Fangmei","family":"Ling","sequence":"first","affiliation":[{"name":"Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan ,","place":["China"]},{"name":"Department of Gastroenterology, The People\u2019s Hospital of Guangxi Zhuang Autonomous Region , Nanning 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