KCa3.1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways

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-β1 signaling...

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Vydané v:	Scientific reports Ročník 6; číslo 1; s. 23884
Hlavní autori:	Huang, Chunling, Lin, Mike Z., Cheng, Delfine, Braet, Filip, Pollock, Carol A., Chen, Xin-Ming
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	London Nature Publishing Group UK 31.03.2016 Nature Publishing Group
Predmet:	1-Phosphatidylinositol 3-kinase 13/1 13/109 13/51 14/19 14/28 14/34 631/80 64/60 692/4022/1585/104 82/29 AKT protein Animals Autophagy Autophagy - genetics Cell Line, Transformed Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetic Nephropathies - chemically induced Diabetic Nephropathies - genetics Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic nephropathy Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Fibrosis Gene Expression Regulation Humanities and Social Sciences Humans Intermediate-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors Intermediate-Conductance Calcium-Activated Potassium Channels - genetics Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - pathology Kidneys Male Mice Mice, Knockout multidisciplinary Nephropathy Nitrotyrosine Oxidative stress Phagocytosis Phagosomes - metabolism Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Rodents Science Signal Transduction siRNA Streptozocin TOR protein TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism Transforming Growth Factor beta1 - pharmacology Transforming growth factor-b1 Vacuoles
ISSN:	2045-2322, 2045-2322
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Abstract	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-β1 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-β1 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-β1 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.
AbstractList	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-β1 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-β1 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-β1 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. 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-β1 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-β1 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-β1 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. 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-β1 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-β1 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-β1 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.
ArticleNumber	23884
Author	Huang, Chunling Cheng, Delfine Lin, Mike Z. Braet, Filip Pollock, Carol A. Chen, Xin-Ming
Author_xml	– sequence: 1 givenname: Chunling surname: Huang fullname: Huang, Chunling organization: Kolling Institute of Medical Research, Sydney Medical School, University of Sydney, Royal North Shore Hospital, St Leonards – sequence: 2 givenname: Mike Z. surname: Lin fullname: Lin, Mike Z. organization: Kolling Institute of Medical Research, Sydney Medical School, University of Sydney, Royal North Shore Hospital, St Leonards – sequence: 3 givenname: Delfine surname: Cheng fullname: Cheng, Delfine organization: School of Medical Sciences (Discipline of Anatomy and Histology) – The Bosch Institute, University of Sydney – sequence: 4 givenname: Filip surname: Braet fullname: Braet, Filip organization: School of Medical Sciences (Discipline of Anatomy and Histology) – The Bosch Institute, University of Sydney, Australian Centre for Microscopy & Microanalysis, Madsen Building, University of Sydney – sequence: 5 givenname: Carol A. surname: Pollock fullname: Pollock, Carol A. organization: Kolling Institute of Medical Research, Sydney Medical School, University of Sydney, Royal North Shore Hospital, St Leonards – sequence: 6 givenname: Xin-Ming surname: Chen fullname: Chen, Xin-Ming organization: Kolling Institute of Medical Research, Sydney Medical School, University of Sydney, Royal North Shore Hospital, St Leonards
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Snippet	Autophagy is emerging as an important pathway in many diseases including diabetic nephropathy. It is acknowledged that oxidative stress plays a critical role...
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StartPage	23884
SubjectTerms	1-Phosphatidylinositol 3-kinase 13/1 13/109 13/51 14/19 14/28 14/34 631/80 64/60 692/4022/1585/104 82/29 AKT protein Animals Autophagy Autophagy - genetics Cell Line, Transformed Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetic Nephropathies - chemically induced Diabetic Nephropathies - genetics Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic nephropathy Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - pathology Fibrosis Gene Expression Regulation Humanities and Social Sciences Humans Intermediate-Conductance Calcium-Activated Potassium Channels - antagonists & inhibitors Intermediate-Conductance Calcium-Activated Potassium Channels - genetics Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - pathology Kidneys Male Mice Mice, Knockout multidisciplinary Nephropathy Nitrotyrosine Oxidative stress Phagocytosis Phagosomes - metabolism Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Rodents Science Signal Transduction siRNA Streptozocin TOR protein TOR Serine-Threonine Kinases - genetics TOR Serine-Threonine Kinases - metabolism Transforming Growth Factor beta1 - pharmacology Transforming growth factor-b1 Vacuoles
Title	KCa3.1 mediates dysfunction of tubular autophagy in diabetic kidneys via PI3k/Akt/mTOR signaling pathways
URI	https://link.springer.com/article/10.1038/srep23884 https://www.ncbi.nlm.nih.gov/pubmed/27029904 https://www.proquest.com/docview/1898688810 https://www.proquest.com/docview/1777988267 https://pubmed.ncbi.nlm.nih.gov/PMC4814925
Volume	6
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