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10.1136/gut.2007.147207 http://scihub22266oqcxt.onion/10.1136/gut.2007.147207 C4551464!4551464!18596195     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Gut 2009 ; 58 (3): 431-42 Nephropedia Template TP {{tp|p=18596195|t=2009. Mechanisms regulating cytochrome c release in pancreatic mitochondria |pdf=|usr=}}{{18596195}} gab.com Text Mechanisms regulating cytochrome c release in pancreatic mitochondria JO: Gut http://www.kidney.de/pget.php?&tw=1&pmid=18596195 #FOAvip Background: Mechanisms of acinar cell death in pancreatitis are poorly understood. Cytochrome c release is a central event in apoptosis in pancreatitis. Here, we assessed the regulation of pancreatic cytochrome c release by Ca2+, mitochondrial membrane potential (??m), and reactive oxygen species (ROS), the signals involved in acute pancreatitis. We used both isolated rat pancreatic mitochondria and intact acinar cells hyper-stimulated with cholecystokinin-8 (CCK-8; in vitro model of acute pancreatitis). Results: Micromolar amounts of Ca2+ depolarised isolated pancreatic mitochondria through a mechanism different from the ?classical? (ie, liver) mitochondrial permeability transition pore (mPTP). In contrast with liver, Ca2+-induced mPTP opening caused a dramatic decrease in ROS and was not associated with pancreatic mitochondria swelling. Importantly, we found that Ca2+-induced depolarisation inhibited cytochrome c release from pancreatic mitochondria, due to blockade of ROS production. As a result, Ca2+ exerted two opposite effects on cytochrome c release: Ca2+ per se stimulated the release, whereas Ca2+-induced depolarisation inhibited it. This dual effect caused a non-monotonous dose-dependence of cytochrome c release on Ca2+. In intact acinar cells, cytochrome c release, caspase activation and apoptosis were all stimulated by ROS and Ca2+, and inhibited by depolarisation, corroborating the findings on isolated pancreatic mitochondria. Conclusions: These data implicate ROS as a key mediator of CCK-induced apoptotic responses. The results indicate a major role for mitochondria in the effects of Ca2+ and ROS on acinar cell death. They suggest that the extent of apoptosis in pancreatitis is regulated by the interplay between ROS, ??m and Ca2+. Stabilising mitochondria against loss of ??m may represent a strategy to mitigate the severity of pancreatitis. Twit Text FOAVip Mechanisms regulating cytochrome c release in pancreatic mitochondria ????Gut http://www.kidney.de/pget.php?&tw=1&pmid=18596195 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18596195 #FOAvip English Wikipedia <ref>{{Cite pmid|18596195}}</ref> Mechanisms regulating cytochrome c release in pancreatic mitochondria #MMPMID18596195 Odinokova I; Sung KF; Mareninova O; Hermann K; Evtodienko Y; Andreyev A; Gukovsky I; Gukovskaya A Gut 2009[Mar]; 58 (3): 431-42 PMID18596195show ga Background: Mechanisms of acinar cell death in pancreatitis are poorly understood. Cytochrome c release is a central event in apoptosis in pancreatitis. Here, we assessed the regulation of pancreatic cytochrome c release by Ca2+, mitochondrial membrane potential (??m), and reactive oxygen species (ROS), the signals involved in acute pancreatitis. We used both isolated rat pancreatic mitochondria and intact acinar cells hyper-stimulated with cholecystokinin-8 (CCK-8; in vitro model of acute pancreatitis). Results: Micromolar amounts of Ca2+ depolarised isolated pancreatic mitochondria through a mechanism different from the ?classical? (ie, liver) mitochondrial permeability transition pore (mPTP). In contrast with liver, Ca2+-induced mPTP opening caused a dramatic decrease in ROS and was not associated with pancreatic mitochondria swelling. Importantly, we found that Ca2+-induced depolarisation inhibited cytochrome c release from pancreatic mitochondria, due to blockade of ROS production. As a result, Ca2+ exerted two opposite effects on cytochrome c release: Ca2+ per se stimulated the release, whereas Ca2+-induced depolarisation inhibited it. This dual effect caused a non-monotonous dose-dependence of cytochrome c release on Ca2+. In intact acinar cells, cytochrome c release, caspase activation and apoptosis were all stimulated by ROS and Ca2+, and inhibited by depolarisation, corroborating the findings on isolated pancreatic mitochondria. Conclusions: These data implicate ROS as a key mediator of CCK-induced apoptotic responses. The results indicate a major role for mitochondria in the effects of Ca2+ and ROS on acinar cell death. They suggest that the extent of apoptosis in pancreatitis is regulated by the interplay between ROS, ??m and Ca2+. Stabilising mitochondria against loss of ??m may represent a strategy to mitigate the severity of pancreatitis. äMechanisms regulating cytochrome c release in pancreatic mitochondria (epmc).pdf DeepDyve Pubget Overpricing