Abstract:
BACKGROUND:Renal fibrosis is a final common pathway of chronic kidney disease. SIRT1, a NAD+-dependent protein deacetylase, deacetylates the p65 of NF-κB and shows protective effects in kidney disorders. miR-373 directly targets the 3'UTR of SIRT1. However, roles of miR-373 in renal fibrosis are unclear. METHODS:TGF-β1, a critical regulator of fibrosis, was used to stimulate human kidney-2 cells to establish cell model for renal fibrosis. Unilateral ureteral obstruction (UUO) was performed as an in vivo model. RESULTS:TGF-β1 induced the level of miR-373, reduced level of SIRT1, and promoted p65 acetylation and MMP-9 expression. These effects were reversed by the miR-373 inhibitor. In the animal model, UUO caused a consistent pattern as demonstrated in vitro. CONCLUSION:These results indicated an undesired effect of miR-373 in the regulation of renal injury and fibrosis by targeting SIRT1-mediated NF-κB/MMP-9 signaling, which might provide a potential therapeutic strategy for renal fibrosis.
journal_name
Genomicsjournal_title
Genomicsauthors
Yang H,Liao D,Tong L,Zhong L,Wu Kdoi
10.1016/j.ygeno.2018.04.017subject
Has Abstractpub_date
2019-07-01 00:00:00pages
786-792issue
4eissn
0888-7543issn
1089-8646pii
S0888-7543(18)30269-6journal_volume
111pub_type
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