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Axelle Cadoret - One of the best experts on this subject based on the ideXlab platform.
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology (Baltimore Md.), 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr−/− mice subjected to Bile Duct ligation (BDL) displayed increased liver damage compared to wildtype BDL mice. Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr−/− BDL mice. Furthermore, evaluation of Vdr−/− BDL mouse liver tissue sections indicated altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr−/− mice subjected to BDL compared to wildtype BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the epidermal growth factor receptor (EGFR) pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr−/− mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (Hepatology 2013;58:1401–1412)
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology, 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr(-/-) mice submitted to Bile Duct ligation (BDL) displayed increased liver damage compared to wild-type BDL mice.Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr(-/-) BDL mice.Furthermore, evaluation of Vdr(-/-) BDL mice liver tissue sectionsindicatedan altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr(-/-) mice submitted to BDL compared to wild-type BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the EGFR pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr(-/-) mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (HEPATOLOGY2013.).
Sung-koo Lee - One of the best experts on this subject based on the ideXlab platform.
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spontaneous Rupture of intrahepatic Bile Duct following portal vein embolization in a patient with perihilar cholangiocarcinoma
한국간담췌외과학회지, 2013Co-Authors: Yong-kyu Chung, Shin Hwang, Young Il Kim, Cheol-min Kang, Dong-il Kwon, Sung-koo LeeAbstract:We herein present a case of spontaneous Rupture of intrahepatic Bile Duct in a patient with perihilar cholangiocarcinoma, which were successfully treated by curative resection. A 60-year-old male patient with perihilar cholangiocarcinoma was decompressed with single percutaneous transhepatic biliary drainage. Two days after right portal vein embolization, the patient suffered from paralytic ileus with marked abdominal distension. Imaging study revealed that marked fluid collection around the liver and whole abdomen, suggesting intrahepatic Bile Duct Rupture. With abdominal drainage and biliary decompression for 2 weeks, the biliary Rupture was controlled. To enhance the safety of right hepatectomy, additional right hepatic vein embolization was performed. The patient underwent routine surgical procedures for right hepatectomy, caudate lobectomy and Bile Duct resection, and recovered uneventfully and discharged 18 days after surgery. This is the first report of a case of spontaneous Rupture of intrahepatic Bile Duct in a patient with perihilar cholangiocarcinoma.
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Spontaneous Rupture of intrahepatic Bile Duct following portal vein embolization in a patient with perihilar cholangiocarcinoma: a case of successful curative resection.
Korean journal of hepato-biliary-pancreatic surgery, 2013Co-Authors: Yong-kyu Chung, Shin Hwang, Young Il Kim, Cheol-min Kang, Dong-il Kwon, Sung-koo LeeAbstract:We herein present a case of spontaneous Rupture of intrahepatic Bile Duct in a patient with perihilar cholangiocarcinoma, which were successfully treated by curative resection. A 60-year-old male patient with perihilar cholangiocarcinoma was decompressed with single percutaneous transhepatic biliary drainage. Two days after right portal vein embolization, the patient suffered from paralytic ileus with marked abdominal distension. Imaging study revealed that marked fluid collection around the liver and whole abdomen, suggesting intrahepatic Bile Duct Rupture. With abdominal drainage and biliary decompression for 2 weeks, the biliary Rupture was controlled. To enhance the safety of right hepatectomy, additional right hepatic vein embolization was performed. The patient underwent routine surgical procedures for right hepatectomy, caudate lobectomy and Bile Duct resection, and recovered uneventfully and discharged 18 days after surgery. This is the first report of a case of spontaneous Rupture of intrahepatic Bile Duct in a patient with perihilar cholangiocarcinoma.
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Efficacy of Percutaneous Cholangioscopic Ethanol Injection in Hepatocellular Carcinoma Invading the Bile Duct
Clinical Endoscopy, 2005Co-Authors: Jung-min Choi, Sung-koo Lee, Sang Soo Lee, Jang-han Lee, Moon-hee Song, Dae-keun Pyun, Tae-jun Song, Jung Sik Choi, Do-hyun Park, Dong-wan SeoAbstract:Background/Aims: To evaluate the clinical outcomes of the percutaneous cholangioscopic ethanol injection in the hepatocellular carcinoma (HCC) invading the Bile Duct, we conDucted a retrospective study. Methods: Ten patients who received the percutaneous cholangioscopic ethanol injection were selected patients were diagnosed as HCC invading the Bile Duct between January 1998 and February 2004. Treatment response, complications, survival or death and survival time were analyzed. Results: Ten patients received mean of 5.3 sessions (range 2-19) of cholangioscopic ethanol injection. Eight patients had decreased tumor mass, and the rest 2 patients had no response. Complications were pain (n=10), hemobilia (n=6: bleeding was minimal), cholangitis (n=2), Bile Duct Rupture (n=1), and Bile Duct stricture (n=1). Nine patients died from severe hepatic failure and sepsis, one patient has survived for 19 months as of now. Median survival time was 5 months (range 2-19 months). Percutaneous transhepatic biliary drainage (PTBD) could be removed in two patients. Conclusions: Percutaneous cholangioscopic ethanol injection in HCC invading the Bile Duct showed size reDuction of mass. PTBD could be no longer needed in some patients. However, supportive cares such as PTBD may be appropriate considering their short survival period and risk of procedure.
Delphine Firrincieli - One of the best experts on this subject based on the ideXlab platform.
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology (Baltimore Md.), 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr−/− mice subjected to Bile Duct ligation (BDL) displayed increased liver damage compared to wildtype BDL mice. Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr−/− BDL mice. Furthermore, evaluation of Vdr−/− BDL mouse liver tissue sections indicated altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr−/− mice subjected to BDL compared to wildtype BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the epidermal growth factor receptor (EGFR) pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr−/− mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (Hepatology 2013;58:1401–1412)
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology, 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr(-/-) mice submitted to Bile Duct ligation (BDL) displayed increased liver damage compared to wild-type BDL mice.Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr(-/-) BDL mice.Furthermore, evaluation of Vdr(-/-) BDL mice liver tissue sectionsindicatedan altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr(-/-) mice submitted to BDL compared to wild-type BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the EGFR pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr(-/-) mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (HEPATOLOGY2013.).
Thomas Braescu - One of the best experts on this subject based on the ideXlab platform.
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology (Baltimore Md.), 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr−/− mice subjected to Bile Duct ligation (BDL) displayed increased liver damage compared to wildtype BDL mice. Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr−/− BDL mice. Furthermore, evaluation of Vdr−/− BDL mouse liver tissue sections indicated altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr−/− mice subjected to BDL compared to wildtype BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the epidermal growth factor receptor (EGFR) pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr−/− mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (Hepatology 2013;58:1401–1412)
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology, 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr(-/-) mice submitted to Bile Duct ligation (BDL) displayed increased liver damage compared to wild-type BDL mice.Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr(-/-) BDL mice.Furthermore, evaluation of Vdr(-/-) BDL mice liver tissue sectionsindicatedan altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr(-/-) mice submitted to BDL compared to wild-type BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the EGFR pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr(-/-) mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (HEPATOLOGY2013.).
Dominique Rainteau - One of the best experts on this subject based on the ideXlab platform.
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology (Baltimore Md.), 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr−/− mice subjected to Bile Duct ligation (BDL) displayed increased liver damage compared to wildtype BDL mice. Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr−/− BDL mice. Furthermore, evaluation of Vdr−/− BDL mouse liver tissue sections indicated altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr−/− mice subjected to BDL compared to wildtype BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the epidermal growth factor receptor (EGFR) pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr−/− mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (Hepatology 2013;58:1401–1412)
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Vitamin D nuclear receptor deficiency promotes cholestatic liver injury by disruption of biliary epithelial cell junctions in mice.
Hepatology, 2013Co-Authors: Delphine Firrincieli, Silvia Zúñiga, Colette Rey, Dominique Wendum, Elisabeth Lasnier, Dominique Rainteau, Thomas Braescu, Thomas Falguières, Mathieu Boissan, Axelle CadoretAbstract:Alterations in apical junctional complexes (AJCs) have been reported in genetic or acquired biliary diseases. The vitamin D nuclear receptor (VDR), predominantly expressed in biliary epithelial cells in the liver, has been shown to regulate AJCs. The aim of our study was thus to investigate the role of VDR in the maintenance of Bile Duct integrity in mice challenged with biliary-type liver injury. Vdr(-/-) mice submitted to Bile Duct ligation (BDL) displayed increased liver damage compared to wild-type BDL mice.Adaptation to cholestasis, ascertained by expression of genes involved in Bile acid metabolism and tissue repair, was limited in Vdr(-/-) BDL mice.Furthermore, evaluation of Vdr(-/-) BDL mice liver tissue sectionsindicatedan altered E-cadherin staining associated with increased Bile Duct Rupture. Total liver protein analysis revealed that a truncated form of E-cadherin was present in higher amounts in Vdr(-/-) mice submitted to BDL compared to wild-type BDL mice. Truncated E-cadherin was also associated with loss of cell adhesion in biliary epithelial cells silenced for VDR. In these cells, E-cadherin cleavage occurred together with calpain 1 activation and was prevented by the silencing of calpain 1. Furthermore, VDR deficiency led to the activation of the EGFR pathway, while EGFR activation by EGF induced both calpain 1 activation and E-cadherin cleavage in these cells. Finally, truncation of E-cadherin was blunted when EGFR signaling was inhibited in VDR-silenced cells. Conclusion: Biliary-type liver injury is exacerbated in Vdr(-/-) mice by limited adaptive response and increased Bile Duct Rupture. These results indicate that loss of VDR restricts the adaptation to cholestasis and diminishes Bile Duct integrity in the setting of biliary-type liver injury. (HEPATOLOGY2013.).