Fig. 5

Cx32 channels regulated the level of miR155-3p induced by I/R or H/R injury. HK-2 cells were seeded at low (25,000 cells/cm²) or high (125,000 cells/cm²) density and subjected to H/R. Bar = 50 μM. A-C Fluorescence in situ hybridization (FISH) was used to observe the level of miR155 (A), miR155-5p (B), and miR155-3p (C) in HK-2 cells in different groups. Con: control group; LD: low density group; HD: high density group. D FISH was used to observe the level of miR155-3p in HK-2 cells at high density in different groups. Con: control group; 2APB: cells were pretreated with 2APB (25 μM) for 1 h before the next step; siRNA: Cx32-siRNA (50 nM) was transfected into cells for 48 h before the next step. Cx32-OP: cells were transfected with plasmid-Cx32 for 48 hours to achieve overexpression of Cx32 before the next step. E Quantitative real-time PCR (RT-qPCR) was used to analyze the expression level of miR-155-3p in renal tissue. WT: wild-type; I/R: ischemia reperfusion; 2APB: mice pretreated with 2APB (inhibitor of Cx32, 20 mg/kg, i.p.) for 1 h before renal ischemia; Cx32^−/−: Cx32 knockout mice. * p < 0.05 vs. sham; # p < 0.05 vs. the WT + IR group. Data are means ± SEM (n = 5)