{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T17:41:55Z","timestamp":1790358115261,"version":"4.1.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2020,7,9]],"date-time":"2020-07-09T00:00:00Z","timestamp":1594252800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2020,7,9]],"date-time":"2020-07-09T00:00:00Z","timestamp":1594252800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Moesin, an ezrin\/radixin\/moesin family member, is involved in the regulation of cell adhesion, polarity, and migration by cross\u2010linking between the actin cytoskeleton and plasma membrane. The primary effector cell in hepatic fibrosis is the hepatic stellate cell (HSC), which undergoes activation during liver injury leading to increased extracellular matrix production.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>Here, we have hypothesized that moesin plays a critical role in linking the HSC cytoskeleton to the fibrogenic cascade during HSC activation. Moesin phosphorylation was up\u2010regulated during HSC activation and fibrogenesis. Using moesin wild\u2010type (WT) and mutant constructs (phosphomimicking T558D and nonphosphorylatable T558A), we found that cellular motility and contraction were increased in moesin WT\u2010infected and T558D\u2010infected cells, paralleled by an increase in smooth muscle \u03b1\u2010actin and collagen 1 expression. In contrast, overexpression of nonphosphorylatable moesin and moesin knockout (KO) decreased cellular motility and contraction. Most importantly, moesin KO led to abrogation of liver fibrosis. The mechanism of moesin's effect was a reduction in myocardin\u2010related transcription factor\u2010A and serum\u2010response factor (SRF)\u2013mediated changes in the actin cytoskeleton, which in turn modulated the expression of matrix genes.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Taken together, our findings suggest that the linkage between cytoskeletal dynamics and the correlated MRTF\/SRF signaling pathway has a pivotal role in HSC activation and fibrogenesis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.31078","type":"journal-article","created":{"date-parts":[[2019,12,20]],"date-time":"2019-12-20T19:06:56Z","timestamp":1576868816000},"page":"1073-1084","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":28,"title":["Moesin, an Ezrin\/Radixin\/Moesin Family Member, Regulates Hepatic Fibrosis"],"prefix":"10.1097","volume":"72","author":[{"given":"Serhan","family":"Karvar","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology,Department of Medicine,Medical University of South Carolina,Charleston,SC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ephraim A.","family":"Ansa\u2010Addo","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology,Hollings Cancer Center,Medical University of South Carolina,Charleston,SC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jo","family":"Suda","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences,Cedars\u2010Sinai Medical Center,Los Angeles,CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shweta","family":"Singh","sequence":"additional","affiliation":[{"name":"Department of Cell and Molecular Pharmacology,Medical University of South Carolina,Charleston,SC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lixin","family":"Zhu","sequence":"additional","affiliation":[{"name":"Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases,Department of Colorectal Surgery,Guangdong Institute of Gastroenterology,The Sixth Affiliated Hospital,Sun Yat\u2010sen University,Guangzhou,China"},{"name":"Department of Biochemistry,University at Buffalo,Buffalo,NY"},{"name":"Department of Pediatrics,University at Buffalo,Buffalo,NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zihai","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology,Hollings Cancer Center,Medical University of South Carolina,Charleston,SC"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Don C.","family":"Rockey","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology,Department of Medicine,Medical University of South Carolina,Charleston,SC"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2020,7,9]]},"reference":[{"key":"hep31078-bib-0001-20241017","doi-asserted-by":"crossref","first-page":"195","DOI":"10.1016\/j.bpg.2011.02.005","article-title":"Mechanisms of hepatic fibrogenesis","volume":"25","year":"2011","journal-title":"Best Pract Res Clin Gastroenterol"},{"key":"hep31078-bib-0002-20241017","doi-asserted-by":"crossref","first-page":"95","DOI":"10.1056\/NEJMc1504848","article-title":"Fibrosis \u2013 a common pathway to organ injury and failure","volume":"373","year":"2015","journal-title":"N Engl J Med"},{"key":"hep31078-bib-0003-20241017","doi-asserted-by":"crossref","first-page":"224","DOI":"10.1016\/j.cgh.2013.01.005","article-title":"Translating an understanding of the pathogenesis of hepatic fibrosis to novel therapies","volume":"11","year":"2013","journal-title":"Clin Gastroenterol 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