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10.1111/jcmm.12859 http://scihub22266oqcxt.onion/10.1111/jcmm.12859 C4988293!4988293!27079462     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       J+Cell+Mol+Med 2016 ; 20 (9): 1664-72 Nephropedia Template TP {{tp|p=27079462|t=2016. Autophagy dysfunction and regulatory cystatin C in macrophage death of atherosclerosis |pdf=|usr=}}{{27079462}} gab.com Text Autophagy dysfunction and regulatory cystatin C in macrophage death of atherosclerosis JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27079462 #FOAvip Autophagy dysfunction in mouse atherosclerosis models has been associated with increased lipid accumulation, apoptosis and inflammation. Expression of cystatin C (CysC) is decreased in human atheroma, and CysC deficiency enhances atherosclerosis in mice. Here, we first investigated the association of autophagy and CysC expression levels with atheroma plaque severity in human atherosclerotic lesions. We found that autophagy proteins Atg5 and LC3? in advanced human carotid atherosclerotic lesions are decreased, while markers of dysfunctional autophagy p62/SQSTM1 and ubiquitin are increased together with elevated levels of lipid accumulation and apoptosis. The expressions of LC3? and Atg5 were positively associated with CysC expression. Second, we investigated whether CysC expression is involved in autophagy in atherosclerotic apoE?deficient mice, demonstrating that CysC deficiency (CysC?/?) in these mice results in reduction of Atg5 and LC3? levels and induction of apoptosis. Third, macrophages isolated from CysC?/? mice displayed increased levels of p62/SQSTM1 and higher sensitivity to 7?oxysterol?mediated lysosomal membrane destabilization and apoptosis. Finally, CysC treatment minimized oxysterol?mediated cellular lipid accumulation. We conclude that autophagy dysfunction is a characteristic of advanced human atherosclerotic lesions and is associated with reduced levels of CysC. The deficiency of CysC causes autophagy dysfunction and apoptosis in macrophages and apoE?deficient mice. The results indicate that CysC plays an important regulatory role in combating cell death via the autophagic pathway in atherosclerosis. Twit Text FOAVip Autophagy dysfunction and regulatory cystatin C in macrophage death of atherosclerosis ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=27079462 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27079462 #FOAvip English Wikipedia <ref>{{Cite pmid|27079462}}</ref> Autophagy dysfunction and regulatory cystatin C in macrophage death of atherosclerosis #MMPMID27079462 Li W; Sultana N; Siraj N; Ward LJ; Pawlik M; Levy E; Jovinge S; Bengtsson E; Yuan X J Cell Mol Med 2016[Sep]; 20 (9): 1664-72 PMID27079462show ga Autophagy dysfunction in mouse atherosclerosis models has been associated with increased lipid accumulation, apoptosis and inflammation. Expression of cystatin C (CysC) is decreased in human atheroma, and CysC deficiency enhances atherosclerosis in mice. Here, we first investigated the association of autophagy and CysC expression levels with atheroma plaque severity in human atherosclerotic lesions. We found that autophagy proteins Atg5 and LC3? in advanced human carotid atherosclerotic lesions are decreased, while markers of dysfunctional autophagy p62/SQSTM1 and ubiquitin are increased together with elevated levels of lipid accumulation and apoptosis. The expressions of LC3? and Atg5 were positively associated with CysC expression. Second, we investigated whether CysC expression is involved in autophagy in atherosclerotic apoE?deficient mice, demonstrating that CysC deficiency (CysC?/?) in these mice results in reduction of Atg5 and LC3? levels and induction of apoptosis. Third, macrophages isolated from CysC?/? mice displayed increased levels of p62/SQSTM1 and higher sensitivity to 7?oxysterol?mediated lysosomal membrane destabilization and apoptosis. Finally, CysC treatment minimized oxysterol?mediated cellular lipid accumulation. We conclude that autophagy dysfunction is a characteristic of advanced human atherosclerotic lesions and is associated with reduced levels of CysC. The deficiency of CysC causes autophagy dysfunction and apoptosis in macrophages and apoE?deficient mice. The results indicate that CysC plays an important regulatory role in combating cell death via the autophagic pathway in atherosclerosis. äAutophagy dysfunction and regulatory cystatin C in macrophage death of(epmc).pdf DeepDyve Pubget Overpricing