Exosomal miRNA-19b-3p of tubular epithelial cells promotes M1 macrophage activation in kidney injury

Tubulointerstitial inflammation is a common characteristic of acute and chronic kidney injury. However, the mechanism by which the initial injury of tubular epithelial cells (TECs) drives interstitial inflammation remains unclear. This paper aims to explore the role of exosomal miRNAs derived from T...

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Vydáno v:	Cell death and differentiation Ročník 27; číslo 1; s. 210 - 226
Hlavní autoři:	Lv, Lin-Li, Feng, Ye, Wu, Min, Wang, Bin, Li, Zuo-Lin, Zhong, Xin, Wu, Wei-Jun, Chen, Jun, Ni, Hai-Feng, Tang, Tao-Tao, Tang, Ri-Ning, Lan, Hui-Yao, Liu, Bi-Cheng
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England Nature Publishing Group 01.01.2020
Témata:	Acute Kidney Injury - genetics Acute Kidney Injury - metabolism Adult Aged Animals Cell activation Cells, Cultured Diabetic Nephropathies - urine Diabetic nephropathy Epithelial cells Epithelial Cells - metabolism Exosomes - genetics Exosomes - metabolism Female Humans Inflammation Kidney - metabolism Kidney - pathology Kidney diseases Kidney Tubules - metabolism Macrophage Activation Macrophages Macrophages - metabolism Male Mice Mice, Inbred BALB C Mice, Inbred C57BL MicroRNAs MicroRNAs - metabolism MicroRNAs - urine Middle Aged miRNA Nephritis - genetics Nephritis - pathology NF-kappa B - metabolism Proteinuria - chemically induced Proteinuria - genetics Proteinuria - metabolism RAW 264.7 Cells Suppressor of Cytokine Signaling 1 Protein - genetics Suppressor of Cytokine Signaling 1 Protein - metabolism
ISSN:	1350-9047, 1476-5403, 1476-5403
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Abstract	Tubulointerstitial inflammation is a common characteristic of acute and chronic kidney injury. However, the mechanism by which the initial injury of tubular epithelial cells (TECs) drives interstitial inflammation remains unclear. This paper aims to explore the role of exosomal miRNAs derived from TECs in the development of tubulointerstitial inflammation. Global microRNA(miRNA) expression profiling of renal exosomes was examined in a LPS induced acute kidney injury (AKI) mouse model and miR-19b-3p was identified as the miRNA that was most notably increased in TEC-derived exosomes compared to controls. Similar results were also found in an adriamycin (ADR) induced chronic proteinuric kidney disease model in which exosomal miR-19b-3p was markedly released. Interestingly, once released, TEC-derived exosomal miR-19b-3p was internalized by macrophages, leading to M1 phenotype polarization through targeting NF-κB/SOCS-1. A dual-luciferase reporter assay confirmed that SOCS-1 was the direct target of miR-19b-3p. Importantly, the pathogenic role of exosomal miR-19b-3p in initiating renal inflammation was revealed by the ability of adoptively transferred of purified TEC-derived exosomes to cause tubulointerstitial inflammation in mice, which was reversed by inhibition of miR-19b-3p. Clinically, high levels of miR-19b-3p were found in urinary exosomes and were correlated with the severity of tubulointerstitial inflammation in patients with diabetic nephropathy. Thus, our studies demonstrated that exosomal miR-19b-3p mediated the communication between injured TECs and macrophages, leading to M1 macrophage activation. The exosome/miR-19b-3p/SOCS1 axis played a critical pathologic role in tubulointerstitial inflammation, representing a new therapeutic target for kidney disease.
AbstractList	Tubulointerstitial inflammation is a common characteristic of acute and chronic kidney injury. However, the mechanism by which the initial injury of tubular epithelial cells (TECs) drives interstitial inflammation remains unclear. This paper aims to explore the role of exosomal miRNAs derived from TECs in the development of tubulointerstitial inflammation. Global microRNA(miRNA) expression profiling of renal exosomes was examined in a LPS induced acute kidney injury (AKI) mouse model and miR-19b-3p was identified as the miRNA that was most notably increased in TEC-derived exosomes compared to controls. Similar results were also found in an adriamycin (ADR) induced chronic proteinuric kidney disease model in which exosomal miR-19b-3p was markedly released. Interestingly, once released, TEC-derived exosomal miR-19b-3p was internalized by macrophages, leading to M1 phenotype polarization through targeting NF-κB/SOCS-1. A dual-luciferase reporter assay confirmed that SOCS-1 was the direct target of miR-19b-3p. Importantly, the pathogenic role of exosomal miR-19b-3p in initiating renal inflammation was revealed by the ability of adoptively transferred of purified TEC-derived exosomes to cause tubulointerstitial inflammation in mice, which was reversed by inhibition of miR-19b-3p. Clinically, high levels of miR-19b-3p were found in urinary exosomes and were correlated with the severity of tubulointerstitial inflammation in patients with diabetic nephropathy. Thus, our studies demonstrated that exosomal miR-19b-3p mediated the communication between injured TECs and macrophages, leading to M1 macrophage activation. The exosome/miR-19b-3p/SOCS1 axis played a critical pathologic role in tubulointerstitial inflammation, representing a new therapeutic target for kidney disease. Tubulointerstitial inflammation is a common characteristic of acute and chronic kidney injury. However, the mechanism by which the initial injury of tubular epithelial cells (TECs) drives interstitial inflammation remains unclear. This paper aims to explore the role of exosomal miRNAs derived from TECs in the development of tubulointerstitial inflammation. Global microRNA(miRNA) expression profiling of renal exosomes was examined in a LPS induced acute kidney injury (AKI) mouse model and miR-19b-3p was identified as the miRNA that was most notably increased in TEC-derived exosomes compared to controls. Similar results were also found in an adriamycin (ADR) induced chronic proteinuric kidney disease model in which exosomal miR-19b-3p was markedly released. Interestingly, once released, TEC-derived exosomal miR-19b-3p was internalized by macrophages, leading to M1 phenotype polarization through targeting NF-κB/SOCS-1. A dual-luciferase reporter assay confirmed that SOCS-1 was the direct target of miR-19b-3p. Importantly, the pathogenic role of exosomal miR-19b-3p in initiating renal inflammation was revealed by the ability of adoptively transferred of purified TEC-derived exosomes to cause tubulointerstitial inflammation in mice, which was reversed by inhibition of miR-19b-3p. Clinically, high levels of miR-19b-3p were found in urinary exosomes and were correlated with the severity of tubulointerstitial inflammation in patients with diabetic nephropathy. Thus, our studies demonstrated that exosomal miR-19b-3p mediated the communication between injured TECs and macrophages, leading to M1 macrophage activation. The exosome/miR-19b-3p/SOCS1 axis played a critical pathologic role in tubulointerstitial inflammation, representing a new therapeutic target for kidney disease.Tubulointerstitial inflammation is a common characteristic of acute and chronic kidney injury. However, the mechanism by which the initial injury of tubular epithelial cells (TECs) drives interstitial inflammation remains unclear. This paper aims to explore the role of exosomal miRNAs derived from TECs in the development of tubulointerstitial inflammation. Global microRNA(miRNA) expression profiling of renal exosomes was examined in a LPS induced acute kidney injury (AKI) mouse model and miR-19b-3p was identified as the miRNA that was most notably increased in TEC-derived exosomes compared to controls. Similar results were also found in an adriamycin (ADR) induced chronic proteinuric kidney disease model in which exosomal miR-19b-3p was markedly released. Interestingly, once released, TEC-derived exosomal miR-19b-3p was internalized by macrophages, leading to M1 phenotype polarization through targeting NF-κB/SOCS-1. A dual-luciferase reporter assay confirmed that SOCS-1 was the direct target of miR-19b-3p. Importantly, the pathogenic role of exosomal miR-19b-3p in initiating renal inflammation was revealed by the ability of adoptively transferred of purified TEC-derived exosomes to cause tubulointerstitial inflammation in mice, which was reversed by inhibition of miR-19b-3p. Clinically, high levels of miR-19b-3p were found in urinary exosomes and were correlated with the severity of tubulointerstitial inflammation in patients with diabetic nephropathy. Thus, our studies demonstrated that exosomal miR-19b-3p mediated the communication between injured TECs and macrophages, leading to M1 macrophage activation. The exosome/miR-19b-3p/SOCS1 axis played a critical pathologic role in tubulointerstitial inflammation, representing a new therapeutic target for kidney disease.
Author	Wu, Min Zhong, Xin Tang, Ri-Ning Liu, Bi-Cheng Feng, Ye Chen, Jun Lan, Hui-Yao Lv, Lin-Li Wang, Bin Ni, Hai-Feng Li, Zuo-Lin Tang, Tao-Tao Wu, Wei-Jun
Author_xml	– sequence: 1 givenname: Lin-Li surname: Lv fullname: Lv, Lin-Li email: lvlinli@seu.edu.cn organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China. lvlinli@seu.edu.cn – sequence: 2 givenname: Ye surname: Feng fullname: Feng, Ye organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 3 givenname: Min surname: Wu fullname: Wu, Min organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 4 givenname: Bin surname: Wang fullname: Wang, Bin organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 5 givenname: Zuo-Lin surname: Li fullname: Li, Zuo-Lin organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 6 givenname: Xin surname: Zhong fullname: Zhong, Xin organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 7 givenname: Wei-Jun surname: Wu fullname: Wu, Wei-Jun organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 8 givenname: Jun surname: Chen fullname: Chen, Jun organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 9 givenname: Hai-Feng surname: Ni fullname: Ni, Hai-Feng organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 10 givenname: Tao-Tao surname: Tang fullname: Tang, Tao-Tao organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 11 givenname: Ri-Ning surname: Tang fullname: Tang, Ri-Ning organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China – sequence: 12 givenname: Hui-Yao orcidid: 0000-0003-4283-9755 surname: Lan fullname: Lan, Hui-Yao organization: Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, and Liu Che Woo Institute of Innovative Medicine, Chinese University of Hong Kong, Hong Kong, SAR, 999077, China – sequence: 13 givenname: Bi-Cheng surname: Liu fullname: Liu, Bi-Cheng email: liubc64@163.com organization: Institute of Nephrology, Zhongda Hospital, Southeast University School of Medicine, Nanjing, Jiangsu Province, 210009, China. liubc64@163.com
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ContentType	Journal Article
Copyright	ADMC Associazione Differenziamento e Morte Cellulare 2019.
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PublicationTitle	Cell death and differentiation
PublicationTitleAlternate	Cell Death Differ
PublicationYear	2020
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Snippet	Tubulointerstitial inflammation is a common characteristic of acute and chronic kidney injury. However, the mechanism by which the initial injury of tubular...
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SubjectTerms	Acute Kidney Injury - genetics Acute Kidney Injury - metabolism Adult Aged Animals Cell activation Cells, Cultured Diabetic Nephropathies - urine Diabetic nephropathy Epithelial cells Epithelial Cells - metabolism Exosomes - genetics Exosomes - metabolism Female Humans Inflammation Kidney - metabolism Kidney - pathology Kidney diseases Kidney Tubules - metabolism Macrophage Activation Macrophages Macrophages - metabolism Male Mice Mice, Inbred BALB C Mice, Inbred C57BL MicroRNAs MicroRNAs - metabolism MicroRNAs - urine Middle Aged miRNA Nephritis - genetics Nephritis - pathology NF-kappa B - metabolism Proteinuria - chemically induced Proteinuria - genetics Proteinuria - metabolism RAW 264.7 Cells Suppressor of Cytokine Signaling 1 Protein - genetics Suppressor of Cytokine Signaling 1 Protein - metabolism
Title	Exosomal miRNA-19b-3p of tubular epithelial cells promotes M1 macrophage activation in kidney injury
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