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Fig. 6 | Molecular Medicine

Fig. 6

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

Fig. 6

ets1 cooperated with KMT5A to regulate PFN2 transcriptional activity in HUVECs. A ets1 and H4K20me1 were enriched at the PFN2 promoter region. B The putative ets1 binding site of PFN2. The motif logo and position weight matrix are shown in the upper and lower panels, respectively. C PFN2 promoter activity was determined by luciferase reporter assays with the corresponding treatment. D Results from the Western blot analysis of KMT5A and PFN2 in the HUVECs with the corresponding treatment. E Compared with the control group, the KMT5A overexpression and mutant KMT5AR259G plasmids both increased KMT5A mRNA expression in HUVECs. F Compared with the control group, KMT5A overexpression decreased PFN2 mRNA expression, while mutant KMT5AR259G did not affect PFN2 mRNA expression. G Results from the Western blot analysis of KMT5A and ets1 in HUVECs with the corresponding treatment. H ets1 overexpression was confirmed by qPCR. I Compared with the control group, ets1 overexpression decreased KMT5A mRNA expression in HUVECs. J Results from the Western blot analysis of KMT5A and ets1 in the HUVECs with the corresponding treatment. K The effects of sh-KMT5A were confirmed by qPCR. L sh-KMT5A increased ets1 mRNA expression in HUVECs. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, n = 5/group)

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