Fig. 5
KMT5A suppression participated in high glucose-mediated EndMT by augmenting PFN2 expression in HUVECs. A Results from the Western blot analysis of KMT5A, PFN2, CD31, vimentin, αSMA and S100A4 in the HUVECs with the corresponding treatment. B The effects of KMT5A overexpression were verified by qPCR. C The high glucose-mediated increase in PFN2 mRNA expression was inhibited by KMT5A overexpression. D The high glucose-mediated decrease in CD31 mRNA expression was counteracted by KMT5A overexpression. E The high glucose-mediated increase in vimentin mRNA expression was inhibited by KMT5A overexpression. F The high glucose-mediated increase in αSMA mRNA expression was inhibited by KMT5A overexpression. G The high glucose-mediated increase in S100A4 mRNA expression was inhibited by KMT5A overexpression. H Results from the Western blot analysis of KMT5A, PFN2, CD31, vimentin, αSMA and S100A4 in the HUVECs with the corresponding treatment. I si-PFN2 did not affect KMT5A mRNA expression. J The effect of si-PFN2 was verified by qPCR. K si-PFN2 upregulated CD31 mRNA expression in sh-KMT5A-treated HUVECs. L si-PFN2 decreased vimentin mRNA expression in sh-KMT5A-treated HUVECs. M si-PFN2 decreased αSMA mRNA expression in sh-KMT5A-treated HUVECs. N si-PFN2 decreased S100A4 mRNA expression in sh-KMT5A-treated HUVECs. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, n = 5/group)