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10.1038/srep23884 http://scihub22266oqcxt.onion/10.1038/srep23884 C4814925!4814925 !27029904     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27029904 &cmd=llinks): Failed to open stream: HTTP request failed! 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KCa3 1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways |pdf=|usr=}}{{27029904 }} gab.com Text KCa3 1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27029904 #FOAvip Autophagy is emerging as an important pathway in many diseases including diabetic nephropathy. It is acknowledged that oxidative stress plays a critical role in autophagy dysfunction and diabetic nephropathy, and KCa3.1 blockade ameliorates diabetic renal fibrosis through inhibiting TGF-?1 signaling pathway. To identify the role of KCa3.1 in dysfunctional tubular autophagy in diabetic nephropathy, human proximal tubular cells (HK2) transfected with scrambled or KCa3.1 siRNAs were exposed to TGF-?1 for 48?h, then autophagosome formation, the autophagy marker LC3, signaling molecules PI3K, Akt and mTOR, and oxidative stress marker nitrotyrosine were examined respectively. In vivo, LC3, nitrotyrosine and phosphorylated mTOR were examined in kidneys of diabetic KCa3.1+/+ and KCa3.1-/- mice. The results demonstrated that TGF-?1 increased the formation of autophagic vacuoles, LC3 expression, and phosphorylation of PI3K, Akt and mTOR in scrambled siRNA transfected HK2 cells compared to control cells, which was reversed in KCa3.1 siRNA transfected HK2 cells. In vivo, expression of LC3 and nitrotyrosine, and phosphorylation of mTOR were significantly increased in kidneys of diabetic KCa3.1+/+ mice compared to non-diabetic mice, which were attenuated in kidneys of diabetic KCa3.1-/- mice. These results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt/mTOR signaling pathways. Twit Text FOAVip KCa3 1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27029904 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27029904 #FOAvip English Wikipedia <ref>{{Cite pmid|27029904 }}</ref> KCa3 1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways #MMPMID27029904 Huang C ; Lin MZ ; Cheng D ; Braet F ; Pollock CA ; Chen XM Sci Rep 2016[Mar]; 6 (ä): 23884 PMID27029904 show ga Autophagy is emerging as an important pathway in many diseases including diabetic nephropathy. It is acknowledged that oxidative stress plays a critical role in autophagy dysfunction and diabetic nephropathy, and KCa3.1 blockade ameliorates diabetic renal fibrosis through inhibiting TGF-?1 signaling pathway. To identify the role of KCa3.1 in dysfunctional tubular autophagy in diabetic nephropathy, human proximal tubular cells (HK2) transfected with scrambled or KCa3.1 siRNAs were exposed to TGF-?1 for 48?h, then autophagosome formation, the autophagy marker LC3, signaling molecules PI3K, Akt and mTOR, and oxidative stress marker nitrotyrosine were examined respectively. In vivo, LC3, nitrotyrosine and phosphorylated mTOR were examined in kidneys of diabetic KCa3.1+/+ and KCa3.1-/- mice. The results demonstrated that TGF-?1 increased the formation of autophagic vacuoles, LC3 expression, and phosphorylation of PI3K, Akt and mTOR in scrambled siRNA transfected HK2 cells compared to control cells, which was reversed in KCa3.1 siRNA transfected HK2 cells. In vivo, expression of LC3 and nitrotyrosine, and phosphorylation of mTOR were significantly increased in kidneys of diabetic KCa3.1+/+ mice compared to non-diabetic mice, which were attenuated in kidneys of diabetic KCa3.1-/- mice. These results suggest that KCa3.1 activation contributes to dysfunctional tubular autophagy in diabetic nephropathy through PI3K/Akt/mTOR signaling pathways. |Animals [MESH] |Autophagy/genetics [MESH] |Cell Line, Transformed [MESH] |Diabetes Mellitus, Experimental/chemically induced/*genetics/metabolism/pathology [MESH] |Diabetic Nephropathies/chemically induced/*genetics/metabolism/pathology [MESH] |Epithelial Cells/drug effects/metabolism/pathology [MESH] |Gene Expression Regulation [MESH] |Humans [MESH] |Intermediate-Conductance Calcium-Activated Potassium Channels/antagonists & inhibitors/*genetics/metabolism [MESH] |Kidney Tubules, Proximal/metabolism/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Phagosomes/metabolism [MESH] |Phosphatidylinositol 3-Kinases/*genetics/metabolism [MESH] |Proto-Oncogene Proteins c-akt/*genetics/metabolism [MESH] |RNA, Small Interfering/genetics/metabolism [MESH] |Signal Transduction [MESH] |Streptozocin [MESH] |TOR Serine-Threonine Kinases/*genetics/metabolism [MESH]KCa3 1 mediates dysfunction of tubular autophagy in diabetic kidneys v(epmc).pdf DeepDyve Pubget Overpricing