ArticleExperimental biology and medicine (Maywood, N.J.)2009
Taurocholate feeding to bile duct ligated rats prevents caffeic acid-induced bile duct damage by changes in cholangiocyte VEGF expression.
Article in Experimental biology and medicine (Maywood, N.J.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Loss of β-catenin in cholangiocytes promotes hepatocyte reprogramming and vascular remodeling during murine cholestasis.Cell communication and signaling : CCS · 2026Article
- Purinergic signaling and cholangiocyte regeneration: a new frontier in ischemic liver injury.Frontiers in transplantation · 2025Review
- Cholangiokines: undervalued modulators in the hepatic microenvironment.Frontiers in immunology · 2023Review
- Article
- New insights on the role of vascular endothelial growth factor in biliary pathophysiology.JHEP reports : innovation in hepatology · 2021Review
- Viral Hepatitis and Iron Dysregulation: Molecular Pathways and the Role of Lactoferrin.Molecules (Basel, Switzerland) · 2020Review
- Regulators of Cholangiocyte Proliferation.Gene expression · 2017Review
- Isolation and characterization of hepatic mast cells from cholestatic rats.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Pathogenesis of Kupffer Cells in Cholestatic Liver Injury.The American journal of pathology · 2016Review
- Ischemia reperfusion of the hepatic artery induces the functional damage of large bile ducts by changes in the expression of angiogenic factors.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Functional and structural features of cholangiocytes in health and disease.Cellular and molecular gastroenterology and hepatology · 2015Article
- Bile acid signaling and biliary functions.Acta pharmaceutica Sinica. B · 2015Review
- Epithelial VEGF signaling is required in the mouse liver for proper sinusoid endothelial cell identity and hepatocyte zonation in vivo.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- The physiological roles of secretin and its receptor.Annals of translational medicine · 2013Review
- Recent advances in the morphological and functional heterogeneity of the biliary epithelium.Experimental biology and medicine (Maywood, N.J.) · 2013Review
- Histamine and histamine receptor regulation of gastrointestinal cancers.Translational gastrointestinal cancer · 2012Article
- Histamine stimulates the proliferation of small and large cholangiocytes by activation of both IP3/Ca2+ and cAMP-dependent signaling mechanisms.Laboratory investigation; a journal of technical methods and pathology · 2012Article
- The efficiency of CAPE on retardation of hepatic fibrosis in biliary obstructed rats.Journal of molecular histology · 2011Article
- Taurocholic acid prevents biliary damage induced by hepatic artery ligation in cholestatic rats.Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2010Article
- Histamine regulation of hyperplastic and neoplastic cell growth in cholangiocytes.World journal of gastrointestinal pathophysiology · 2010Article
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
unlabelledCholangiocytes are the target cells in cholestatic models of ductal hyperplasia including bile duct ligation (BDL). We have shown that: (i) cholangiocytes express VEGFR-2 and VEGFR-3; (ii) VEGF-A and VEGF-C stimulate cholangiocyte proliferation via an autocrine mechanism; and (iii) chronic administration of VEGF-A prevents cholangiocyte damage induced by hepatic artery ligation. Caffeic acid phenethyl ester (CAPE) induces growth inhibition in different cells. Taurocholic acid (TC) protects cholangiocytes against injury induced by parasympathetic or sympathetic denervation. The aims of this study were to determine if: (i) CAPE induces bile duct damage; and (ii) TC prevents CAPE-induced bile duct damage by increasing cholangiocyte VEGF expression.
methodsNormal and BDL rats (immediately after surgery) were fed 1% TC or control diet in the absence/presence of daily IP injections of CAPE (10 mg/Kg BW). One week later, we evaluated: (i) cholangiocyte apoptosis, proliferation and ductal mass in liver sections; (ii) functional activity by measuring secretin-stimulated bile and bicarbonate secretion; and (iii) VEGF-A/C and VEGFR-2/R-3 expression in liver sections. In vitro, BDL cholangiocytes were exposed to CAPE (40 microM) in the absence/presence of TC (40 microM) with and without pretreatment with VEGF receptor inhibitors before evaluating cholangiocyte apoptosis and proliferation.
resultsChronic CAPE administration to BDL rats increased cholangiocyte apoptosis and decreased ductal mass. This effect was associated with reduced expression of VEGF-A, VEGF-C, VEGFR-2 and VEGFR-3. In vivo, TC feeding partly prevented CAPE-induced changes in cholangiocyte apoptosis and growth and loss of ductal secretion. The protective effect of TC was associated with enhanced VEGF-A, VEGF-C, VEGFR-2 and VEGFR-3. In vitro, TC partially prevented CAPE-induced increases in apoptosis and decreases in cholangiocyte proliferation. These changes were reversed by pretreatment with VEGF-receptor inhibitors.
conclusionManipulation of cholangiocyte VEGF expression by bile acids may be important in preventing the impairment of cholangiocyte proliferation by exogenous agents.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.