A KDM6A–KLF10 reinforcing feedback mechanism aggravates diabetic podocyte dysfunction
Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that K...
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| Published in | EMBO molecular medicine Vol. 11; no. 5; pp. 1 - n/a |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.05.2019
EMBO Press John Wiley and Sons Inc Springer Nature |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1757-4676 1757-4684 1757-4684 |
| DOI | 10.15252/emmm.201809828 |
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| Abstract | Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up‐regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte‐specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes‐induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both
KDM6A
and
KLF10
proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A–KLF10 feedback loop may be beneficial to attenuate diabetes‐induced kidney injury.
Synopsis
Podocyte dysfunction is an early event in the development of diabetic nephropathy. This study reveals that activation of a KDM6A‐KLF10 positive feedback loop by hyperglycemia critically contributes to podocyte dysfunction. Blocking the KDM6A‐KLF10 signaling axis ameliorates diabetic kidney injury.
Both KDM6A and KLF10 are up‐regulated in podocytes under diabetic conditions.
Activation of the positive inter‐regulation between KDM6A and KLF10 results in repression of multiple podocyte‐specific marker proteins.
Inactivation or podocyte‐specific knockout of KDM6A in mice attenuates diabetes‐induced kidney injury.
Kidney injury is also reduced in KLF10‐knockout mice under diabetic conditions.
Elevated levels of urinary exosomal KDM6A and KLF10 mRNAs are observed in human diabetic nephropathy patients relative to control subjects.
Graphical Abstract
Podocyte dysfunction is an early event in the development of diabetic nephropathy. This study reveals that activation of a KDM6A‐KLF10 positive feedback loop by hyperglycemia critically contributes to podocyte dysfunction. Blocking the KDM6A‐KLF10 signaling axis ameliorates diabetic kidney injury. |
|---|---|
| AbstractList | Abstract Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up‐regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte‐specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes‐induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both KDM6A and KLF10 proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A–KLF10 feedback loop may be beneficial to attenuate diabetes‐induced kidney injury. Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up‐regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte‐specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes‐induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both KDM6A and KLF10 proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A–KLF10 feedback loop may be beneficial to attenuate diabetes‐induced kidney injury. Synopsis Podocyte dysfunction is an early event in the development of diabetic nephropathy. This study reveals that activation of a KDM6A‐KLF10 positive feedback loop by hyperglycemia critically contributes to podocyte dysfunction. Blocking the KDM6A‐KLF10 signaling axis ameliorates diabetic kidney injury. Both KDM6A and KLF10 are up‐regulated in podocytes under diabetic conditions. Activation of the positive inter‐regulation between KDM6A and KLF10 results in repression of multiple podocyte‐specific marker proteins. Inactivation or podocyte‐specific knockout of KDM6A in mice attenuates diabetes‐induced kidney injury. Kidney injury is also reduced in KLF10‐knockout mice under diabetic conditions. Elevated levels of urinary exosomal KDM6A and KLF10 mRNAs are observed in human diabetic nephropathy patients relative to control subjects. Graphical Abstract Podocyte dysfunction is an early event in the development of diabetic nephropathy. This study reveals that activation of a KDM6A‐KLF10 positive feedback loop by hyperglycemia critically contributes to podocyte dysfunction. Blocking the KDM6A‐KLF10 signaling axis ameliorates diabetic kidney injury. Diabetic nephropathy is the leading cause of end-stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up-regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte-specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes-induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both and proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A-KLF10 feedback loop may be beneficial to attenuate diabetes-induced kidney injury. Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM 6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up‐regulation of its downstream target KLF 10. Overexpression of KLF 10 in podocytes not only represses multiple podocyte‐specific markers including nephrin, but also conversely increases KDM 6A expression. We further show that KLF 10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM 6A or KLF 10 in mice significantly suppresses diabetes‐induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both KDM 6A and KLF 10 proteins or mRNA s are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM 6A– KLF 10 feedback loop may be beneficial to attenuate diabetes‐induced kidney injury. Diabetic nephropathy is the leading cause of end-stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up-regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte-specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes-induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both KDM6A and KLF10 proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A-KLF10 feedback loop may be beneficial to attenuate diabetes-induced kidney injury.Diabetic nephropathy is the leading cause of end-stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up-regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte-specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes-induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both KDM6A and KLF10 proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A-KLF10 feedback loop may be beneficial to attenuate diabetes-induced kidney injury. Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up‐regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte‐specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes‐induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both KDM6A and KLF10 proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A–KLF10 feedback loop may be beneficial to attenuate diabetes‐induced kidney injury. Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is critically associated with diabetic nephropathy, the mechanism underlying podocyte dysfunction still remains obscure. Here, we identify that KDM6A, a histone lysine demethylase, reinforces diabetic podocyte dysfunction by creating a positive feedback loop through up‐regulation of its downstream target KLF10. Overexpression of KLF10 in podocytes not only represses multiple podocyte‐specific markers including nephrin, but also conversely increases KDM6A expression. We further show that KLF10 inhibits nephrin expression by directly binding to the gene promoter together with the recruitment of methyltransferase Dnmt1. Importantly, inactivation or knockout of either KDM6A or KLF10 in mice significantly suppresses diabetes‐induced proteinuria and kidney injury. Consistent with the notion, we also show that levels of both KDM6A and KLF10 proteins or mRNAs are substantially elevated in kidney tissues or in urinary exosomes of human diabetic nephropathy patients as compared with control subjects. Our findings therefore suggest that targeting the KDM6A–KLF10 feedback loop may be beneficial to attenuate diabetes‐induced kidney injury. Synopsis Podocyte dysfunction is an early event in the development of diabetic nephropathy. This study reveals that activation of a KDM6A‐KLF10 positive feedback loop by hyperglycemia critically contributes to podocyte dysfunction. Blocking the KDM6A‐KLF10 signaling axis ameliorates diabetic kidney injury. Both KDM6A and KLF10 are up‐regulated in podocytes under diabetic conditions. Activation of the positive inter‐regulation between KDM6A and KLF10 results in repression of multiple podocyte‐specific marker proteins. Inactivation or podocyte‐specific knockout of KDM6A in mice attenuates diabetes‐induced kidney injury. Kidney injury is also reduced in KLF10‐knockout mice under diabetic conditions. Elevated levels of urinary exosomal KDM6A and KLF10 mRNAs are observed in human diabetic nephropathy patients relative to control subjects. Podocyte dysfunction is an early event in the development of diabetic nephropathy. This study reveals that activation of a KDM6A‐KLF10 positive feedback loop by hyperglycemia critically contributes to podocyte dysfunction. Blocking the KDM6A‐KLF10 signaling axis ameliorates diabetic kidney injury. |
| Author | Lin, Chun‐Liang Shih, Ya‐Hsueh Huang, Yu‐Ting Chiang, Wen‐Chih Chang, Pey‐Jium Hsu, Yung‐Chien Wang, Ching‐Jen |
| AuthorAffiliation | 4 Kidney and Diabetic Complications Research Team (KDCRT) Chang Gung Memorial Hospital Chiayi Taiwan 8 Graduate Institute of Clinical Medical Sciences College of Medicine Chang Gung University Taoyuan Taiwan 3 College of Medicine Chang Gung University Taoyuan Taiwan 6 Department of Orthopedic Surgery Chang Gung Memorial Hospital Kaohsiung Taiwan 7 Department of Internal Medicine National Taiwan University Hospital Taipei Taiwan 1 Departments of Nephrology Chang Gung Memorial Hospital Chiayi Taiwan 2 Kidney Research Center Chang Gung Memorial Hospital Taipei Taiwan 5 Center for Shockwave Medicine and Tissue Engineering Department of Medical Research Chang Gung Memorial Hospital Kaohsiung Taiwan |
| AuthorAffiliation_xml | – name: 1 Departments of Nephrology Chang Gung Memorial Hospital Chiayi Taiwan – name: 5 Center for Shockwave Medicine and Tissue Engineering Department of Medical Research Chang Gung Memorial Hospital Kaohsiung Taiwan – name: 4 Kidney and Diabetic Complications Research Team (KDCRT) Chang Gung Memorial Hospital Chiayi Taiwan – name: 7 Department of Internal Medicine National Taiwan University Hospital Taipei Taiwan – name: 3 College of Medicine Chang Gung University Taoyuan Taiwan – name: 6 Department of Orthopedic Surgery Chang Gung Memorial Hospital Kaohsiung Taiwan – name: 8 Graduate Institute of Clinical Medical Sciences College of Medicine Chang Gung University Taoyuan Taiwan – name: 2 Kidney Research Center Chang Gung Memorial Hospital Taipei Taiwan |
| Author_xml | – sequence: 1 givenname: Chun‐Liang surname: Lin fullname: Lin, Chun‐Liang organization: Departments of Nephrology, Chang Gung Memorial Hospital, Kidney Research Center, Chang Gung Memorial Hospital, College of Medicine, Chang Gung University, Kidney and Diabetic Complications Research Team (KDCRT), Chang Gung Memorial Hospital, Center for Shockwave Medicine and Tissue Engineering, Department of Medical Research, Chang Gung Memorial Hospital – sequence: 2 givenname: Yung‐Chien surname: Hsu fullname: Hsu, Yung‐Chien organization: Departments of Nephrology, Chang Gung Memorial Hospital, Kidney and Diabetic Complications Research Team (KDCRT), Chang Gung Memorial Hospital – sequence: 3 givenname: Yu‐Ting surname: Huang fullname: Huang, Yu‐Ting organization: Departments of Nephrology, Chang Gung Memorial Hospital, Kidney and Diabetic Complications Research Team (KDCRT), Chang Gung Memorial Hospital – sequence: 4 givenname: Ya‐Hsueh surname: Shih fullname: Shih, Ya‐Hsueh organization: Departments of Nephrology, Chang Gung Memorial Hospital, Kidney and Diabetic Complications Research Team (KDCRT), Chang Gung Memorial Hospital – sequence: 5 givenname: Ching‐Jen surname: Wang fullname: Wang, Ching‐Jen organization: Center for Shockwave Medicine and Tissue Engineering, Department of Medical Research, Chang Gung Memorial Hospital, Department of Orthopedic Surgery, Chang Gung Memorial Hospital – sequence: 6 givenname: Wen‐Chih surname: Chiang fullname: Chiang, Wen‐Chih organization: Department of Internal Medicine, National Taiwan University Hospital – sequence: 7 givenname: Pey‐Jium orcidid: 0000-0002-6492-0346 surname: Chang fullname: Chang, Pey‐Jium email: peyjiumc@mail.cgu.edu.tw organization: Departments of Nephrology, Chang Gung Memorial Hospital, Kidney and Diabetic Complications Research Team (KDCRT), Chang Gung Memorial Hospital, Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30948420$$D View this record in MEDLINE/PubMed |
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| Keywords | KLF10 podocyte dysfunction diabetic nephropathy epigenetics KDM6A |
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| References | 2007; 104 1997; 236 2017; 8 2012; 287 2013; 28 2007; 106 2018; 128 2010; 108 2011; 60 2007; 581 2003; 14 2014; 25 2007; 71 2013; 242 2014; 63 2012; 488 2016; 186 2009; 12 2014; 5 2010; 24 2010; 114 1995; 23 2000; 11 2015; 88 2015; 87 2013; 110 2012; 27 2014; 9 2010; 6 2014; 124 2011; 2 2010; 36 2017; 60 2005; 353 2017; 28 2015; 125 2013; 45 2017; 21 2010a; 59 2006b; 101 2009; 297 2006a; 39 2003; 290 2014; 86 2002; 25 2016; 6 2002; 161 2015; 29 2004; 15 2002; 21 1999; 30 2017; 144 2010b; 21 2007; 87 2010; 90 2018; 10 2006; 103 e_1_2_10_23_1 e_1_2_10_46_1 e_1_2_10_21_1 e_1_2_10_44_1 e_1_2_10_42_1 e_1_2_10_40_1 e_1_2_10_2_1 e_1_2_10_4_1 e_1_2_10_18_1 e_1_2_10_53_1 e_1_2_10_6_1 e_1_2_10_16_1 e_1_2_10_39_1 e_1_2_10_55_1 e_1_2_10_8_1 e_1_2_10_14_1 e_1_2_10_37_1 e_1_2_10_57_1 e_1_2_10_58_1 e_1_2_10_13_1 e_1_2_10_34_1 e_1_2_10_11_1 e_1_2_10_32_1 e_1_2_10_30_1 e_1_2_10_51_1 e_1_2_10_61_1 e_1_2_10_29_1 e_1_2_10_27_1 e_1_2_10_25_1 e_1_2_10_48_1 e_1_2_10_24_1 e_1_2_10_45_1 e_1_2_10_22_1 e_1_2_10_43_1 e_1_2_10_20_1 e_1_2_10_41_1 e_1_2_10_52_1 e_1_2_10_3_1 e_1_2_10_19_1 e_1_2_10_54_1 e_1_2_10_5_1 e_1_2_10_17_1 e_1_2_10_38_1 e_1_2_10_56_1 e_1_2_10_7_1 e_1_2_10_15_1 e_1_2_10_36_1 e_1_2_10_12_1 e_1_2_10_35_1 e_1_2_10_9_1 e_1_2_10_59_1 e_1_2_10_10_1 e_1_2_10_33_1 e_1_2_10_31_1 e_1_2_10_50_1 e_1_2_10_60_1 e_1_2_10_28_1 e_1_2_10_49_1 e_1_2_10_26_1 e_1_2_10_47_1 |
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| Snippet | Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is... Diabetic nephropathy is the leading cause of end-stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial cells, is... Abstract Diabetic nephropathy is the leading cause of end‐stage renal disease. Although dysfunction of podocytes, also termed glomerular visceral epithelial... |
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| SubjectTerms | Animals Base Sequence Cell Line, Transformed Deoxyribonucleic acid Diabetes Diabetes mellitus Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic Nephropathies - physiopathology Diabetic Nephropathies - urine Diabetic nephropathy DNA DNA methylation DNMT1 protein Down-Regulation Early Growth Response Transcription Factors - genetics Early Growth Response Transcription Factors - metabolism EMBO21 EMBO45 Enzymes Epigenesis, Genetic Epigenetics Epithelial cells Exosomes Exosomes - metabolism Experiments Feedback Feedback, Physiological Gene expression Histone Demethylases - genetics Histone Demethylases - metabolism Hospitals Humans KDM6A Kidney - metabolism Kidney - pathology Kidney - physiopathology Kidneys KLF10 Kruppel-Like Transcription Factors - genetics Kruppel-Like Transcription Factors - metabolism Laboratory animals Lysine Male Medical research Membrane Proteins - metabolism Methyltransferase Mice, Inbred C57BL Mice, Knockout Nephropathy Phenotype podocyte dysfunction Podocytes - metabolism Podocytes - pathology Promoter Regions, Genetic - genetics Protein Binding Proteins Proteinuria Renal function Research Article Signal transduction |
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| Title | A KDM6A–KLF10 reinforcing feedback mechanism aggravates diabetic podocyte dysfunction |
| URI | https://link.springer.com/article/10.15252/emmm.201809828 https://onlinelibrary.wiley.com/doi/abs/10.15252%2Femmm.201809828 https://www.ncbi.nlm.nih.gov/pubmed/30948420 https://www.proquest.com/docview/2268371521 https://www.proquest.com/docview/2204692933 https://pubmed.ncbi.nlm.nih.gov/PMC6505577 https://doaj.org/article/857ba0a3fcf7453187994e965aa68f7c |
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