{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T14:22:48Z","timestamp":1792592568713,"version":"4.5.0"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>Regulation of TF (tissue factor):FVIIa (coagulation factor VIIa) complex procoagulant activity is especially critical in tissues where plasma can contact TF-expressing cells. One example is the liver, where hepatocytes are routinely exposed to plasma because of the fenestrated sinusoidal endothelium. Although liver-associated TF contributes to coagulation, the mechanisms controlling the TF:FVIIa complex activity in this tissue are not known.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Approach and Results:<\/jats:title>\n                    <jats:p>\n                      Common bile duct ligation in mice triggered rapid hepatocyte TF-dependent intrahepatic coagulation coincident with increased plasma bile acids, which occurred at a time before observable liver damage. Similarly, plasma TAT (thrombin-antithrombin) levels increased in cholestatic patients without concurrent hepatocellular injury. Pathologically relevant concentrations of the bile acid glycochenodeoxycholic acid rapidly increased hepatocyte TF-dependent procoagulant activity in vitro, independent of de novo TF synthesis and necrotic or apoptotic cell death. Glycochenodeoxycholic acid increased hepatocyte TF activity even in the presence of the phosphatidylserine-blocking protein lactadherin. Interestingly, glycochenodeoxycholic acid and taurochenodeoxycholic acid increased the procoagulant activity of the TF:FVIIa complex relipidated in unilamellar phosphatidylcholine vesicles, which was linked to an apparent decrease in the K\n                      <jats:sub>m<\/jats:sub>\n                      for FX (coagulation factor X). Notably, the zwitterionic detergent 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, a bile acid structural analog, did not increase relipidated TF:FVIIa activity. Bile acids directly enhanced factor X activation by recombinant soluble TF:FVIIa complex but had no effect on FVIIa alone.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>The results indicate that bile acids directly accelerate TF:FVIIa\u2013driven coagulation reactions, suggesting a novel mechanism whereby elevation in a physiological mediator can directly increase TF:FVIIa procoagulant activity.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.119.313215","type":"journal-article","created":{"date-parts":[[2019,8,15]],"date-time":"2019-08-15T05:00:46Z","timestamp":1565845246000},"page":"2038-2048","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":18,"title":["Direct Amplification of Tissue Factor:Factor VIIa Procoagulant Activity by Bile Acids Drives Intrahepatic Coagulation"],"prefix":"10.1161","volume":"39","author":[{"given":"Kevin S.","family":"Baker","sequence":"first","affiliation":[{"name":"From the Department of Pharmacology and Toxicology (K.S.B., J.P.L.), Michigan State University, East Lansing"},{"name":"Institute for Integrative Toxicology (K.S.B., A.K.K., J.P.L.), Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna K.","family":"Kopec","sequence":"additional","affiliation":[{"name":"Institute for Integrative Toxicology (K.S.B., A.K.K., J.P.L.), Michigan State University, East Lansing"},{"name":"Department of Pathobiology and Diagnostic Investigation (A.K.K., A.P. L.G.P., H.C.-F., D.I., J.P.L.), Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Asmita","family":"Pant","sequence":"additional","affiliation":[{"name":"Department of Pathobiology and Diagnostic Investigation (A.K.K., A.P. L.G.P., H.C.-F., D.I., J.P.L.), Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren G.","family":"Poole","sequence":"additional","affiliation":[{"name":"Department of Pathobiology and Diagnostic Investigation (A.K.K., A.P. L.G.P., H.C.-F., D.I., J.P.L.), Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Holly","family":"Cline-Fedewa","sequence":"additional","affiliation":[{"name":"Department of Pathobiology and Diagnostic Investigation (A.K.K., A.P. L.G.P., H.C.-F., D.I., J.P.L.), Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dora","family":"Ivkovich","sequence":"additional","affiliation":[{"name":"Department of Pathobiology and Diagnostic Investigation (A.K.K., A.P. 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