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Fig. 3 | Molecular Medicine

Fig. 3

From: ets1 associates with KMT5A to participate in high glucose-mediated EndMT via upregulation of PFN2 expression in diabetic nephropathy

Fig. 3

ets1 participated in high glucose-induced EndMT by augmenting PFN2 expression in HUVECs. A Results from the Western blot analysis of ets1, PFN2, CD31, vimentin, αSMA and S100A4 in the HUVECs with the corresponding treatment. B The effects of si-ets1 were confirmed by qPCR. C Compared with high-glucose treatment, si-ets1 decreased PFN2 mRNA expression in hyperglycemic HUVECs. D Compared with high-glucose treatment, si-ets1 increased CD31 mRNA expression in hyperglycemic HUVECs. E Compared with high-glucose treatment, si-ets1 decreased vimentin mRNA expression in hyperglycemic HUVECs. F Compared with high-glucose treatment, si-ets1 decreased αSMA mRNA expression in hyperglycemic HUVECs. G Compared with high-glucose treatment, si-ets1 decreased S100A4 mRNA expression in hyperglycemic HUVECs. H Results from the Western blot analysis of ets1, PFN2, CD31, vimentin, αSMA and S100A4 in the HUVECs with the corresponding treatment. I The effects of ets1 overexpression were confirmed by qPCR. J The effects of si-PFN2 were confirmed by qPCR. K ets1 overexpression inhibited CD31 mRNA expression, which was reversed by si-PFN2 treatment. L ets1 overexpression increased vimentin mRNA expression, which was reversed by si-PFN2 treatment. M ets1 overexpression increased αSMA mRNA expression, which was reversed by si-PFN2 treatment. N ets1 overexpression increased S100A4 mRNA expression, which was reversed by si-PFN2 treatment. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, n = 5/group)

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