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10.1042/BSR20170869 http://scihub22266oqcxt.onion/10.1042/BSR20170869 C5700272!5700272!29046367     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       Biosci+Rep 2017 ; 37 (6): ä Nephropedia Template TP {{tp|p=29046367|t=2017. PKC? silencing alleviates saturated fatty acid induced ER stress by enhancing SERCA activity |pdf=|usr=}}{{29046367}} gab.com Text PKC silencing alleviates saturated fatty acid induced ER stress by enhancing SERCA activity JO: Biosci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29046367 #FOAvip Protein kinase C ? (PKC?) plays an important role in nonalcoholic fatty liver disease (NAFLD), however, the mechanism remains unknown. The present study explored the role of PKC? in NAFLD development and investigated the relationships between PKC?, calcium homeostasis, and endoplasmic reticulum (ER) stress (ERS). Hepatic steatosis cell model was induced by palmitic acid (PA) in L02 cells. Lipid accretion was evaluated using Oil Red O staining and a triglyceride (TG) detection kit. PKC? was down-regulated by siRNA. RT-PCR and Western blotting were used to detect the expression of ERS markers. The fluorescence of Ca2+ influx was recorded using confocal microscopy. Sarco-ER Ca2+-ATPase (SERCA) activity was measured by ultramicro-ATP enzyme test kit. PA treatment induced lipid accretion in L02 cells, destroyed the ER structure, and increased PKC? activation in a time-dependent manner. Further, PA treatment significantly increased the expression of ERS markers, Ig heavy chain binding protein (Bip), and homologous proteins of CCAAT-enhancer binding proteins (CHOP). PKC? silencing down-regulated Bip and CHOP expression, indicating a successful alleviation of ERS. The increased calcium storage induced by PA stimulation was significantly decreased in L02 cells treated with PKC? siRNA compared with the negative control. Moreover, diminished SERCA activity caused by PA was recovered in PKC? siRNA transfected cells. To the best of our knowledge, this is the first report demonstrating that the inhibition of PKC? alleviates ERS by enhancing SERCA activity and stabilizing calcium homeostasis. Twit Text FOAVip PKC silencing alleviates saturated fatty acid induced ER stress by enhancing SERCA activity ????Biosci Rep http://www.kidney.de/pget.php?&tw=1&pmid=29046367 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29046367 #FOAvip English Wikipedia <ref>{{Cite pmid|29046367}}</ref> PKC? silencing alleviates saturated fatty acid induced ER stress by enhancing SERCA activity #MMPMID29046367 Lai S; Li Y; Kuang Y; Cui H; Yang Y; Sun W; Liu K; Chen D; Yan Q; Wen L Biosci Rep 2017[Dec]; 37 (6): ä PMID29046367show ga Protein kinase C ? (PKC?) plays an important role in nonalcoholic fatty liver disease (NAFLD), however, the mechanism remains unknown. The present study explored the role of PKC? in NAFLD development and investigated the relationships between PKC?, calcium homeostasis, and endoplasmic reticulum (ER) stress (ERS). Hepatic steatosis cell model was induced by palmitic acid (PA) in L02 cells. Lipid accretion was evaluated using Oil Red O staining and a triglyceride (TG) detection kit. PKC? was down-regulated by siRNA. RT-PCR and Western blotting were used to detect the expression of ERS markers. The fluorescence of Ca2+ influx was recorded using confocal microscopy. Sarco-ER Ca2+-ATPase (SERCA) activity was measured by ultramicro-ATP enzyme test kit. PA treatment induced lipid accretion in L02 cells, destroyed the ER structure, and increased PKC? activation in a time-dependent manner. Further, PA treatment significantly increased the expression of ERS markers, Ig heavy chain binding protein (Bip), and homologous proteins of CCAAT-enhancer binding proteins (CHOP). PKC? silencing down-regulated Bip and CHOP expression, indicating a successful alleviation of ERS. The increased calcium storage induced by PA stimulation was significantly decreased in L02 cells treated with PKC? siRNA compared with the negative control. Moreover, diminished SERCA activity caused by PA was recovered in PKC? siRNA transfected cells. To the best of our knowledge, this is the first report demonstrating that the inhibition of PKC? alleviates ERS by enhancing SERCA activity and stabilizing calcium homeostasis. äPKC? silencing alleviates saturated fatty acid induced ER stress by en(epmc).pdf DeepDyve Pubget Overpricing