Open AccessMiR-214 promotes renal fibrosis in diabetic nephropathy via targeting SOCS1
Author(s) -
Weiwei Xi,
Xuming Zhao,
Meijun Wu,
Xueqin Fu,
Wenhao Jia,
Mingxi Lu,
Hua Li
Publication year - 2021
Publication title -
tropical journal of pharmaceutical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.209
H-Index - 36
eISSN - 1596-5996
pISSN - 1596-9827
DOI - 10.4314/tjpr.v18i5.14
Subject(s) - fibrosis , diabetic nephropathy , suppressor of cytokine signaling 1 , pathogenesis , downregulation and upregulation , kidney , blot , nephropathy , transfection , cytokine , chemistry , cancer research , medicine , microbiology and biotechnology , endocrinology , biology , diabetes mellitus , gene , suppressor , biochemistry
Purpose: To elucidate how miR-214 regulates the pathogenesis of diabetic nephropathy (DN).
Methods: The extent of fibrosis in DN mice kidneys was examined using Masson’s staining. Quantitative polymerase chain reaction (qPCR) was used to determine the levels of miR-214. Dual luciferase reporter assay was used to identify the target of miR-214. The expression of fibrosis marker proteins of high glucose-stimulated NRK-52E cells transfected with miR-214 was determined using western blotting.
Results: Fibrosis in renal tissue of DN mice was significantly increased and miR-214 was upregulated (p < 0.001). Suppressor of cytokine signaling 1 protein (SOCS1) was the target gene of miR-214, and overexpression of miR-214 promoted fibrosis (p < 0.05, p < 0.001). On the other hand, overexpression of SOCS1 inhibited this process, indicating that miR-214 promoted fibrosis via targeting SOCS1 (p < 0.001). Finally, inhibition of miR-214 c ameliorated renal fibrosis in DN mice (p < 0.01, p < 0.001).
Conclusions: MiR-214 is upregulated in db/db DN mice kidney tissue; miR-214 regulates renal fibrosis in DN mice by targeting SOCS1.