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10.1053/j.gastro.2009.11.047 http://scihub22266oqcxt.onion/10.1053/j.gastro.2009.11.047 C4794984!4794984!19944696     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Gastroenterology 2010 ; 138 (3): 1134-42 Nephropedia Template TP {{tp|p=19944696|t=2010. Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor dependent manner |pdf=|usr=}}{{19944696}} gab.com Text Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor dependent manner JO: Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=19944696 #FOAvip Background and aims: Hepatitis C virus (HCV) infection leads to progressive liver disease, frequently culminating in fibrosis and hepatocellular carcinoma. The mechanisms underlying liver injury in chronic hepatitis C are poorly understood. This study evaluated the role of vascular endothelial growth factor (VEGF) in hepatocyte polarity and HCV infection. Methods: We utilized polarized hepatoma cell lines and the recently described infectious HCV JFH-1 cell culture system to study the role of VEGF in regulating hepatoma permeability and HCV infection. Results: VEGF negatively regulates hepatocellular tight junction (TJ) integrity and cell polarity by a novel VEGF receptor 2 dependent pathway. VEGF reduced hepatoma TJ integrity, induced a re-organization of occludin and promoted HCV entry. Conversely, inhibition of hepatoma expressed VEGF with the receptor kinase inhibitor Sorafenib or with neutralizing anti-VEGF antibodies promoted polarization and inhibited HCV entry, demonstrating an autocrine pathway. HCV infection of primary hepatocytes or hepatoma cell lines promoted VEGF expression and reduced their polarity. Importantly, treatment of HCV infected cells with VEGF inhibitors restored their ability to polarize, demonstrating a VEGF-dependent pathway. Conclusion: Hepatic polarity is critical to normal liver physiology. HCV infection promotes VEGF expression that depolarizes hepatoma cells, promoting viral transmission and lymphocyte migration into the parenchyma that may promote hepatocyte injury. Twit Text FOAVip Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor dependent manner ????Gastroenterology http://www.kidney.de/pget.php?&tw=1&pmid=19944696 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19944696 #FOAvip English Wikipedia <ref>{{Cite pmid|19944696}}</ref> Hepatitis C virus infection reduces hepatocellular polarity in a vascular endothelial growth factor dependent manner #MMPMID19944696 Mee CJ; Farquhar MJ; Harris HJ; Ramma W; Ahmed A; Maurel P; Bicknell R; Balfe P; McKeating JA Gastroenterology 2010[Mar]; 138 (3): 1134-42 PMID19944696show ga Background and aims: Hepatitis C virus (HCV) infection leads to progressive liver disease, frequently culminating in fibrosis and hepatocellular carcinoma. The mechanisms underlying liver injury in chronic hepatitis C are poorly understood. This study evaluated the role of vascular endothelial growth factor (VEGF) in hepatocyte polarity and HCV infection. Methods: We utilized polarized hepatoma cell lines and the recently described infectious HCV JFH-1 cell culture system to study the role of VEGF in regulating hepatoma permeability and HCV infection. Results: VEGF negatively regulates hepatocellular tight junction (TJ) integrity and cell polarity by a novel VEGF receptor 2 dependent pathway. VEGF reduced hepatoma TJ integrity, induced a re-organization of occludin and promoted HCV entry. Conversely, inhibition of hepatoma expressed VEGF with the receptor kinase inhibitor Sorafenib or with neutralizing anti-VEGF antibodies promoted polarization and inhibited HCV entry, demonstrating an autocrine pathway. HCV infection of primary hepatocytes or hepatoma cell lines promoted VEGF expression and reduced their polarity. Importantly, treatment of HCV infected cells with VEGF inhibitors restored their ability to polarize, demonstrating a VEGF-dependent pathway. Conclusion: Hepatic polarity is critical to normal liver physiology. HCV infection promotes VEGF expression that depolarizes hepatoma cells, promoting viral transmission and lymphocyte migration into the parenchyma that may promote hepatocyte injury. äHepatitis C virus infection reduces hepatocellular polarity in a vascu(epmc).pdf DeepDyve Pubget Overpricing