Fig. 5
From: PRMT3 methylates HIF-1α to enhance the vascular calcification induced by chronic kidney disease
PRMT3 knockdown inhibits the β-GP-induced calcification and glycolysis by the downregualtion of HIF-1α in VSMCs
VSMCs were co-infected with adenovirus Ad-shPRMT3/Ad-NCshRNA (shown as PRMT3(−)/NC) and Ad-HIF-1α/Vector (shown as HIF-1α(+)/Vec). Next, cells were incubated with 10 mM β-GP. (A-D) Protein levels of HIF-1α, α-SMA, and OPN in VSMCs. (E) mRNA expression of RUNX2. (F) ALP content. (G) Alizarin Red S staining was performed to evaluate the calcification of VSMCs. Scale bar is 100 μm. (H) Lactic acid content. (I-J) Protein expression of GLUT1 and PKM2. Data is represented as mean ± SD. p < 0.05, p < 0.01 vs. β-GP + PRMT3(−) + Vec. ALP: alkaline phosphatase; β-GP: β-glycerophosphate; GLUT1: glucose transporter type 1; HIF-1α: hypoxia inducible factor 1 subunit alpha; NC: negative control; PKM2: pyruvate kinase M1/2; PRMT3: protein arginine methyltransferase 3; VSMCs: vascular smooth muscle cells