title: MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.
abstract: MiR-155 has been reported to be involved in both innate and adaptive immune responses. But the role of miR-155 in hyperglycemia-induced nephropathy is still unknown. In our current study, 3-month-old male wild-type C57 mice and Mir-155(-/-) mice were used to establish hyperglycemia-induced nephropathy. In our hyperglycemia-induced nephropathy model, the expression of podocyte injury marker desmin was markedly increased in the diabetes group when compared with control. Diabetes also significantly decreased the levels of nephrin and acetylated nephrin, whereas the expression of miR-155 was markedly increased in diabetes group when compared with control. MiR-155(-/-) mice showed significantly increased expression of nephrin, acetylated nephrin, and Wilm's tumor-1 protein (WT-1) when compared with wild-type control. MiR-155 deficiency results in significantly decrease in IL-17A expression both in vivo and in vitro. And the increased expression of WT-1, nephrin, and ac-nephrin was reversed with additional treatment of rmIL-17. Furthermore, we found that the inhibited Th17 differentiation induced by miR-155 deficiency was dependent on increased expression of SOCS1. In conclusion, miR-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy. This was associated with inhibited IL-17 production through enhancement of SOCS1 expression.
authors: Department of Nephrology, the Affiliated Hospital of Youjiang Medical University for Nationalities, 18 Zhongshan Road, Baise, China.
authors: Xu
authors: X
authors: Lin
authors: Yanwu
authors: Y
authors: You
authors: Jie
authors: J
authors: Wang
authors: Youling
authors: Y
authors: Qin
authors: Peng
authors: P
authors: Huang
authors: Fafen
authors: F
authors: Yang
mesh_terms: D000107:Acetylation; D058186:Acute Kidney Injury / Q000139:chemically induced / Q000235:genetics*; D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects; D003893:Desmin / Q000096:biosynthesis; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology; D003928:Diabetic Nephropathies / Q000139:chemically induced / Q000235:genetics*; D006943:Hyperglycemia / Q000139:chemically induced / Q000235:genetics* / Q000503:physiopathology; D020381:Interleukin-17 / Q000096:biosynthesis; D007668:Kidney / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D035683:MicroRNAs / Q000235:genetics*; D050199:Podocytes / Q000473:pathology; D012097:Repressor Proteins / Q000096:biosynthesis / Q000378:metabolism; D013311:Streptozocin; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000096:biosynthesis; D058504:Th17 Cells / Q000166:cytology; D025721:WT1 Proteins
chemical_list: D003893:Desmin; C098680:Il17a protein, mouse; D020381:Interleukin-17; D008565:Membrane Proteins; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; D012097:Repressor Proteins; C491590:Socs1 protein, mouse; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D025721:WT1 Proteins; C000602896:WT1 protein, mouse; C113267:nephrin; D013311:Streptozocin