{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T02:49:22Z","timestamp":1790563762627,"version":"4.1.0"},"reference-count":46,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T00:00:00Z","timestamp":1571356800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T00:00:00Z","timestamp":1571356800000},"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":[[2020,3]]},"abstract":"<jats:sec>\n            <jats:title>Background and Aims<\/jats:title>\n            <jats:p>Serotonin (5HT) is a neuroendocrine hormone synthetized in the central nervous system (CNS) as well as enterochromaffin cells of the gastrointestinal tract. Tryptophan hydroxylase (TPH1) and monoamine oxidase (MAO\u2010A) are the key enzymes for the synthesis and catabolism of 5HT, respectively. Previous studies demonstrated that 5\u2010hydroxytryptamine receptor (5HTR)1A\/1B receptor agonists inhibit biliary hyperplasia in bile\u2010duct ligated (BDL) rats, whereas 5HTR2B receptor antagonists attenuate liver fibrosis (LF) in mice. Our aim was to evaluate the role of 5HTR2A\/2B\/2C agonists\/antagonists in cholestatic models.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results<\/jats:title>\n            <jats:p>While <jats:italic toggle=\"yes\">in vivo<\/jats:italic> studies were performed in BDL rats and the multidrug resistance gene 2 knockout (<jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic>) mouse model of PSC, <jats:italic toggle=\"yes\">in vitro<\/jats:italic> studies were performed in cell lines of cholangiocytes and hepatic stellate cells (HSCs). 5HTR2A\/2B\/2C and MAO\u2010A\/TPH1 are expressed in cholangiocytes and HSCs from BDL rats and <jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic>\n                                 <jats:sup>\u2010<\/jats:sup> mice. Ductular reaction, LF, as well as the mRNA expression of proinflammatory genes increased in normal, BDL rats, and <jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic>\n                                 <jats:sup>\u2010<\/jats:sup> mice following treatment 5HTR2A\/2B\/2C agonists, but decreased when BDL rats and <jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic> mice were treated with 5HTR2A\/2B\/2C antagonists compared to BDL rats and <jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic> mice, respectively. 5HT levels increase in <jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic> mice and in PSC human patients compared to their controls and decrease in serum of <jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic> mice treated with 5HTR2A\/2B\/2C antagonists compared to untreated <jats:italic toggle=\"yes\">Mdr2\u2013\/\u2013\n                                 <\/jats:italic> mice. <jats:italic toggle=\"yes\">In vitro<\/jats:italic>, cell lines of murine cholangiocytes and human HSCs express 5HTR2A\/2B\/2C and MAO\u2010A\/TPH1; treatment of these cell lines with 5HTR2A\/2B\/2C antagonists or TPH1 inhibitor decreased 5HT levels as well as expression of fibrosis and inflammation genes compared to controls.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Modulation of the TPH1\/MAO\u2010A\/5HT\/5HTR2A\/2B\/2C axis may represent a therapeutic approach for management of cholangiopathies, including PSC.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.30880","type":"journal-article","created":{"date-parts":[[2019,7,25]],"date-time":"2019-07-25T20:59:43Z","timestamp":1564088383000},"page":"990-1008","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":40,"title":["Modulation of the Tryptophan Hydroxylase 1\/Monoamine Oxidase\u2010A\/5\u2010Hydroxytryptamine\/5\u2010Hydroxytryptamine Receptor 2A\/2B\/2C Axis Regulates Biliary Proliferation and Liver Fibrosis During Cholestasis"],"prefix":"10.1097","volume":"71","author":[{"given":"Konstantina","family":"Kyritsi","sequence":"first","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana University School of Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lixian","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology,Texas A&M University College of Medicine,Bryan,TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"April","family":"O\u2019Brien","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology,Texas A&M University College of Medicine,Bryan,TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heather","family":"Francis","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana University School of Medicine,Indianapolis,IN"},{"name":"Indiana University School of Medicine,Research, Richard L. Roudebush VA Medical Center,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Travis W.","family":"Hein","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology,Texas A&M University College of Medicine,Bryan,TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Venter","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana University School of Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nan","family":"Wu","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana University School of Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ludovica","family":"Ceci","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana University School of Medicine,Indianapolis,IN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianhao","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology,Texas A&M University College of Medicine,Bryan,TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Zawieja","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology,Texas A&M University College of Medicine,Bryan,TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anatoliy A.","family":"Gashev","sequence":"additional","affiliation":[{"name":"Department of Medical Physiology,Texas A&M University College of Medicine,Bryan,TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fanyin","family":"Meng","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology and Hepatology, Department of Medicine,Indiana University School of Medicine,Indianapolis,IN"},{"name":"Indiana University School of Medicine,Research, Richard L. 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