1. miR-384-5p通过阻断BMP7转录后调控促进肾纤维化.
- Author
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张文静, 孙吉平, 吕 佳, 李 燕, 耿瀛洲, 邵耀中, 尹爱萍, and 路万虹
- Abstract
Objective To investigate whether microRNA-384-5p can interfere with renal fibrosis by regulating BMP7 transcription in renal tubular epithelial cells. Methods Unilateral ureteral obstructive (UUO) model was established, and fluorescence activated cell sorter (FACS) was used to isolate renal tubular epithelial cells for culture. Plasmid expressing miR-384-5p, antisense miR-384-5p, and blank plasmid were transfected by liposome and injected in UUO mice. Masson staining was used to detect renal fibrosis, and Western blot and real-time PCR were used to detect the expressions of target-genes of miRNA (miR-384-5p, miR-30, miR-92, and miR-128). Results There was obvious renal fibrosis at 14 day in UUO model group; the expression of BMP7 mRNA in the renal tissue increased obviously while the expression of BMP7 protein was not increased. Although miR-384-5p could not change BMP7 mRNA in the renal tubular epithelial cells, BMP7 protein in the renal tubular epithelial cells that overexpressed miR-384-5p decreased significantly, and BMP7 protein in these cells overexpressing antisense miR- 384-5p increased significantly. Immunohistochemistry and quantitative PCR showed that renal tissue fibrosis in UUO mice increased significantly in 14 days, while antisense miR-384-5p could significantly reduce the renal tissue fibrosis. Although antisense-miR-384-5p treatment did not affect the level of BMP7 mRNA, it could significantly increase the expression of BMP7 protein in renal tissue, suggesting that inhibiting miR-384-5p could lessen renal injury in UUO mice. Conclusion As a key factor regulating the mechanism of renal fibrosis after renal injury, targeting miR-384-5p may become a new method to prevent and treat renal fibrosis. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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