{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T13:38:15Z","timestamp":1791293895838,"version":"4.1.0"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"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":[[2016,10]]},"abstract":"<jats:p>Hepatic fibrosis is marked by activation of hepatic stellate cells (HSCs). Cholestatic injury precedes liver fibrosis, and cholangiocytes interact with HSCs promoting fibrosis. Mast cells (MCs) infiltrate following liver injury and release histamine, increasing biliary proliferation. We evaluated if inhibition of MC\u2010derived histamine decreases biliary proliferation and fibrosis. Wild\u2010type and multidrug resistance 2 knockout mice (9\u201011 weeks) were treated with cromolyn sodium for 1 week to block MC\u2010derived histamine. Biliary mass and proliferation were evaluated by immunohistochemistry for cytokeratin 19 and Ki\u201067. Bile flow, bicarbonate excretion, and total bile acids were measured in all mice. Fibrosis was evaluated by sirius red\/fast green staining and by quantitative polymerase chain reaction for alpha\u2010smooth muscle actin, fibronectin, collagen type 1a, and transforming growth factor\u2010beta 1. HSC activation was evaluated by quantitative polymerase chain reaction in total liver and immunofluorescent staining in tissues for synaptophysin 9. Histamine serum secretion was measured by enzymatic immunoassay. Mouse liver and human liver samples from control or primary sclerosing cholangitis patients were evaluated for MC markers by quantitative polymerase chain reaction and immunohistochemistry. <jats:italic toggle=\"yes\">In vitro,<\/jats:italic> cultured MCs were transfected with histidine decarboxylase short hairpin RNA to decrease histamine secretion and subsequently cocultured with cholangiocytes or HSCs prior to measuring fibrosis markers, proliferation, and transforming growth factor\u2010beta 1 secretion. Treatment with cromolyn sodium decreased biliary proliferation, fibrosis, histamine secretion, and bile flow in multidrug resistance 2 knockout mice. Primary sclerosing cholangitis mice and patients have increased MCs. Knockdown of MC histidine decarboxylase decreased cholangiocyte and HSC proliferation\/activation. <jats:italic toggle=\"yes\">Conclusion<\/jats:italic>: MCs are recruited to proliferating cholangiocytes and promote fibrosis. Inhibition of MC\u2010derived histamine decreases fibrosis, and regulation of MC mediators may be therapeutic for primary sclerosing cholangitis. (H<jats:sc>epatology<\/jats:sc> 2016;64:1202\u20101216)<\/jats:p>","DOI":"10.1002\/hep.28704","type":"journal-article","created":{"date-parts":[[2016,6,28]],"date-time":"2016-06-28T23:07:01Z","timestamp":1467155221000},"page":"1202-1216","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":79,"title":["Inhibition of mast cell\u2010secreted histamine decreases biliary proliferation and fibrosis in primary sclerosing cholangitis Mdr2\u2212\/\u2212 mice"],"prefix":"10.1097","volume":"64","author":[{"given":"Hannah","family":"Jones","sequence":"first","affiliation":[{"name":"Scott & White Digestive Disease Research Center,Baylor Scott & White Health,Temple,TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Hargrove","sequence":"additional","affiliation":[{"name":"Scott & White Digestive Disease Research Center,Baylor Scott & White 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