ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2015
Ischemia reperfusion of the hepatic artery induces the functional damage of large bile ducts by changes in the expression of angiogenic factors.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Arterial and biliary complications after transarterial chemoembolization for hepatocellular carcinoma.World journal of clinical oncology · 2026Review
- Consensus classification of biliary complications after liver transplantation: guidelines from the BileducTx meeting.The British journal of surgery · 2025Article
- Cholangiocyte Organoids in Liver Transplantation; a Comprehensive Review.Transplant international : official journal of the European Society for Organ Transplantation · 2024Review
- Expression and role of cocaine-amphetamine regulated transcript (CART) in the proliferation of biliary epithelium.European journal of histochemistry : EJH · 2023Article
- Prediction of bile duct injury after transarterial chemoembolization for hepatocellular carcinoma: Model establishment and verification.Frontiers in oncology · 2022Article
- Viral Hepatitis and Iron Dysregulation: Molecular Pathways and the Role of Lactoferrin.Molecules (Basel, Switzerland) · 2020Review
- Liver repair and regeneration after ischemia-reperfusion injury is associated with prolonged fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Liver transplantation and cholangiocarcinoma induce biliary dysfunction following ischemia reperfusion (IR). The function of the intrahepatic biliary tree is regulated by both autocrine and paracrine factors. The aim of the study was to demonstrate that IR-induced damage of cholangiocytes is associated with altered expression of biliary angiogenic factors. Normal and bile duct ligation rats underwent 24-h sham or hepatic reperfusion after 30 min of transient occlusion of the hepatic artery (HAIR) or portal vein (PVIR) before collecting liver blocks and cholangiocyte RNA or protein. We evaluated liver histology, biliary apoptosis, proliferation and expression of VEGF-A/C, VEGFR-2/3, Ang-1/2, and Tie-1/2 in liver sections and isolated small and large cholangiocytes. Normal rat intrahepatic cholangiocyte cultures (NRICC) were maintained under standard conditions in normoxic or under a hypoxic atmosphere for 4 h and then transferred to normal conditions for selected times. Subsequently, we measured changes in biliary proliferation and apoptosis and the expression of VEGF-A/C and VEGFR-2/3. In vivo, HAIR (but not PVIR) induced damage of large bile ducts and decreased proliferation and secretin-stimulated cAMP levels. HAIR-induced damage of large bile ducts was associated with increased expression of VEGF-A/C, VEGFR-2/3, Ang-1/2, and Tie-1/2. In vitro, under hypoxic conditions, there was increased apoptosis and reduced proliferation of NRICC concomitant with enhanced expression of VEGF-A/C and VEGFR-2/3. The functional damage of large bile ducts by HAIR and hypoxia is associated with increased expression of angiogenic factors in small cholangiocytes, presumably due to a compensatory mechanism in response to biliary damage.
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