Fig. 7: 1700020I14Rik reduced the expressions of fibrosis factors in MCs by regulating miR-34a-5p/Sirt1/HIF-1α signaling. | Cell Death & Disease

Fig. 7: 1700020I14Rik reduced the expressions of fibrosis factors in MCs by regulating miR-34a-5p/Sirt1/HIF-1α signaling.

From: LincRNA 1700020I14Rik alleviates cell proliferation and fibrosis in diabetic nephropathy via miR-34a-5p/Sirt1/HIF-1α signaling

Fig. 7

a–b Protein expression levels of Sirt1 and HIF-1α in MCs influenced by 1700020I14Rik plasmids (a) and by siRNA (b) were tested by western blot. c, d Protein expressions of Sirt1 and HIF-1α regulated by the effect of 1700020I14Rik combined with miR-34a-5p mimics (c) or inhibitor (d) were tested by western blot. These results indicated that 1700020I14Rik regulates the expressions of Sirt1 and HIF-1α by regulating miR-34a-5p. e, f Protein expression levels of Col-4, FN, and TGF-β1 regulated by the effect of 1700020I14Rik combined with miR-34a-5p mimics (e) or inhibitor (f) were measured by western blot. Results showed that the expressions of renal fibrosis genes TGF-β1, FN, and Col-4 were reduced by overexpression of 1700020I14Rik, the expressions of these proteins were abolished by the participation of miR-34a-5p mimics. The expressions of TGF-β1, FN, and Col-4 were upregulated by silence of 1700020I14Rik, these changes were blocked by miR-34a-5p inhibitor. Data were represented as the mean ± SD of three independent experiments. *p < 0.05; **p < 0.01, and ***p < 0.001, n.s: no statistical significance

Back to article page