Fig. 3

HIF-1α upregulates miR-182 and then promotes Th17 cell differentiation. a miR-182 expression in Th17 cells determined by RT-qPCR; b the HIF-1α protein expression by Western blot analysis and the effect of HIF-1α on the miR-182 promoter activity detected by dual luciferase reporter gene assay; c the binding of HIF-1α to miR-182 promoter detected by ChIP assay; d miR-182 expression after HIF-1α/YAP overexpression or knockdown determined by RT-qPCR; e Th17 cell proportion after different treatments detected by flow cytometry; f the level of IL-17A in cell supernatant after different treatments determined by ELISA; g RORγt mRNA expression in cells after different treatments determined by RT-qPCR; h Western blot analysis of RORγt protein in cells after different treatments. Comparisons between two groups were conducted by unpaired t test, and those between multiple groups were conducted by one-way ANOVA with Tukey’s post hoc test; the experiments were repeated 3 times independently; * p < 0.05, compared with the normal individuals (normal), normal mice (normal-M), CD4⁺ T cells, cells treated with sh-NC, oe-NC, oe-NC + inhibitor-NC, or sh-NC + mimic-NC; # p < 0.05, compared with the cells treated with oe-HIF-1α + inhibitor-NC or sh-HIF-1α + mimic-NC; & p < 0.05, compared with the cells treated with oe-YAP + inhibitor-NC or sh-YAP + mimic-NC. n = 22 in normal individuals; n = 29 in asthma patients; n = 12 in normal mice; n = 12 in asthma mice