Tauroursodeoxycholic acid activates protein kinase C in isolated rat hepatocytes
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Ursodeoxycholic acid in pregnancy?
2019, Journal of HepatologyRole of Bile Acids and the Biliary HCO <inf>3</inf><sup>−</sup> Umbrella in the Pathogenesis of Primary Biliary Cholangitis
2018, Clinics in Liver DiseaseCitation Excerpt :TMEM16A regulates anion permeability via protein kinase C alpha (PKCα)- and Ca2+-dependent mechanisms, leading to the dominant chloride gradient that drives AE2-mediated Cl−/HCO3− exchange.45 UDCA, the standard treatment for patients with PBC, which is also applied in various other cholestatic liver diseases owing to its potent anticholestatic effects, stimulates PKCα- and Ca2+-dependent Cl− and HCO3− secretion of cholangiocytes via activation of TMEM16A,42,46 a mechanism of action similar to that unraveled for hepatocytes 2 decades ago.47–50 Insulin receptors are localized in the apical membrane of cholangiocytes and are activated by insulin and insulin-like growth factor present in bile.51
Bile Formation and the Enterohepatic Circulation
2018, Physiology of the Gastrointestinal Tract, Sixth EditionTauroursodeoxycholic acid prevents stress induced aggregation of proteins in vitro and promotes PERK activation in HepG2 cells
2015, Archives of Biochemistry and BiophysicsNew paradigms in the treatment of hepatic cholestasis: From UDCA to FXR, PXR and beyond
2015, Journal of HepatologyCitation Excerpt :Early after the first peer-reviewed reports on UDCA in PBC [7,8] it was proposed that UDCA exerts its hepatoprotective effects in cholestatic liver disease mainly by stimulating impaired hepatobiliary secretion [30]. In the 1990’s, UDCA was then unraveled as a potent intracellular signaling molecule acting as a Ca2+ agonist [31–34] and an activator of protein kinase C (cPKCα) [35–37], mitogen-activated protein kinases (MAPK: Erk1/2, p38MAPK) [38,39] and α5β1 integrins [40,41] in hepatocytes. It was earlier proposed [33,42] and later experimentally proven that UDCA conjugates as potent signaling molecules that might stimulate secretion of hepatocytes (and cholangiocytes [43]) by activating vesicular exocytosis and carrier insertion into their apical membranes resulting in choleretic effects via a dual MAPK- and integrin-dependent mechanism in healthy liver [39,40] and in anticholestatic effects via Ca2+-/type II inositol-1,3,4-triphosphate receptor/cPKCα/PKA-dependent mechanisms in cholestatic liver [44–46].