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10.1002/hep.28724 http://scihub22266oqcxt.onion/10.1002/hep.28724 C5033699!5033699!27396550     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hepatology 2016 ; 64 (4): 1317-29 Nephropedia Template TP {{tp|p=27396550|t=2016. Liver kinase B1 regulates hepatocellular tight junction distribution and function in vivo |pdf=|usr=}}{{27396550}} gab.com Text Liver kinase B1 regulates hepatocellular tight junction distribution and function in vivo JO: Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=27396550 #FOAvip Liver kinase B1 (LKB1) and its downstream effector AMP?activated protein kinase (AMPK) play critical roles in polarity establishment by regulating membrane trafficking and energy metabolism. In collagen sandwich?cultured hepatocytes, loss of LKB1 or AMPK impaired apical ABCB11 (Bsep) trafficking and bile canalicular formation. In the present study, we used liver?specific (albumin?Cre) LKB1 knockout mice (LKB1?/?) to investigate the role of LKB1 in the maintenance of functional tight junction (TJ) in vivo. Transmission electron microscopy examination revealed that hepatocyte apical membrane with microvilli substantially extended into the basolateral domain of LKB1?/? livers. Immunofluorescence studies revealed that loss of LKB1 led to longer and wider canalicular structures correlating with mislocalization of the junctional protein, cingulin. To test junctional function, we used intravital microscopy to quantify the transport kinetics of 6?carboxyfluorescein diacetate (6?CFDA), which is processed in hepatocytes into its fluorescent derivative 6?carboxyfluorescein (6?CF) and secreted into the canaliculi. In LKB1?/? mice, 6?CF remained largely in hepatocytes, canalicular secretion was delayed, and 6?CF appeared in the blood. To test whether 6?CF was transported through permeable TJ, we intravenously injected low molecular weight (3 kDa) dextran in combination with 6?CFDA. In wild?type mice, 3 kDa dextran remained in the vasculature, whereas it rapidly appeared in the abnormal bile canaliculi in LKB1?/? mice, confirming that junctional disruption resulted in paracellular exchange between the blood stream and the bile canaliculus. Conclusion: LKB1 plays a critical role in regulating the maintenance of TJ and paracellular permeability, which may explain how various drugs, chemicals, and metabolic states that inhibit the LKB1/AMPK pathway result in cholestasis. (Hepatology 2016;64:1317?1329) Twit Text FOAVip Liver kinase B1 regulates hepatocellular tight junction distribution and function in vivo ????Hepatology http://www.kidney.de/pget.php?&tw=1&pmid=27396550 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27396550 #FOAvip English Wikipedia <ref>{{Cite pmid|27396550}}</ref> Liver kinase B1 regulates hepatocellular tight junction distribution and function in vivo #MMPMID27396550 Porat?Shliom N; Tietgens AJ; Van Itallie CM; Vitale?Cross L; Jarnik M; Harding OJ; Anderson JM; Gutkind JS; Weigert R; Arias IM Hepatology 2016[Oct]; 64 (4): 1317-29 PMID27396550show ga Liver kinase B1 (LKB1) and its downstream effector AMP?activated protein kinase (AMPK) play critical roles in polarity establishment by regulating membrane trafficking and energy metabolism. In collagen sandwich?cultured hepatocytes, loss of LKB1 or AMPK impaired apical ABCB11 (Bsep) trafficking and bile canalicular formation. In the present study, we used liver?specific (albumin?Cre) LKB1 knockout mice (LKB1?/?) to investigate the role of LKB1 in the maintenance of functional tight junction (TJ) in vivo. Transmission electron microscopy examination revealed that hepatocyte apical membrane with microvilli substantially extended into the basolateral domain of LKB1?/? livers. Immunofluorescence studies revealed that loss of LKB1 led to longer and wider canalicular structures correlating with mislocalization of the junctional protein, cingulin. To test junctional function, we used intravital microscopy to quantify the transport kinetics of 6?carboxyfluorescein diacetate (6?CFDA), which is processed in hepatocytes into its fluorescent derivative 6?carboxyfluorescein (6?CF) and secreted into the canaliculi. In LKB1?/? mice, 6?CF remained largely in hepatocytes, canalicular secretion was delayed, and 6?CF appeared in the blood. To test whether 6?CF was transported through permeable TJ, we intravenously injected low molecular weight (3 kDa) dextran in combination with 6?CFDA. In wild?type mice, 3 kDa dextran remained in the vasculature, whereas it rapidly appeared in the abnormal bile canaliculi in LKB1?/? mice, confirming that junctional disruption resulted in paracellular exchange between the blood stream and the bile canaliculus. Conclusion: LKB1 plays a critical role in regulating the maintenance of TJ and paracellular permeability, which may explain how various drugs, chemicals, and metabolic states that inhibit the LKB1/AMPK pathway result in cholestasis. (Hepatology 2016;64:1317?1329) äLiver kinase B1 regulates hepatocellular tight junction distribution a(epmc).pdf DeepDyve Pubget Overpricing