Fig. 6

H19 facilitates wound healing in diabetic mice by activating HIF-1α signaling pathway. a RT-qPCR detection showing that expression of HIF-1α was significantly increased in response to H19 overexpression and si-HIF-1α co-transfection; b EDU staining (× 400) showing that fibroblast proliferation was inhibited in response to H19 overexpression and si-HIF-1α co-transfection; scale bar = 25 μm; c western blot analysis showing that the expression of activation related proteins (FAP, Col1A1 and α-SMA) in fibroblasts was significantly decreased in response to H19 overexpression and si-HIF-1α co-transfection; d wound healing speed was reduced in response to si-HIF-1α lentiviral injection; N = 8; e immunohistochemical staining (× 400) showing that number of fibroblasts was reduced in response to si-HIF-1α lentiviral injection; scale bar = 25 μm; N = 8; f western blot analysis showing that the expression of wound healing related proteins (VEGF, SDF, SCF, MMP-1, MMP-2 and MMP-3) was reduced; g Masson staining (× 400) showing that collagen content of skin tissue of diabetic mice was decreased; scale bar = 25 μm; N = 8; h western blot analysis showing that the expression of fibroblast activation related protein (FAP, Col1A1 and α-SMA) was reduced; *, p < 0.05, compared with the NC group; The above results were measurement data, which were presented as the mean ± standard deviation. Comparisons between two groups were analyzed by t-test. The speed of wound healing was analyzed by two-way analysis of variance. The experiment was repeated 3 times; RT-qPCR, reverse transcription quantitative polymerase chain reaction; HIF-1α, hypoxia-inducible factor-1α; DM, diabetes mellitus; EDU, ethynyl-2′-deoxyuridine; NC, negative control; VEGF, vascular endothelial growth factor; SDF, stromal cell-derived factor; SCF, stem cell factor; MMP, matrix metalloproteinase; α-SMA, α-smooth muscle actin