[Knockdown of PCSK9 inhibits endothelial-to-mesenchymal transition of human aortic endothelial cells].

Objective To investigate the protective effect of proprotein convertase subtilisin/kexin type 9 (PCSK9) knockdown on endothelial-to-mesenchymal transition (EndoMT) induced by β glycerophosphate, dexamethasone, and L-ascorbic acid in human aortic endothelial cells (HAECs). Methods EndoMT model was established by inducing HAECs with (0, 10, 30, 50) mmol/L of β glycerophosphate combined with 100 nmol/L of dexamethasone and 50 μg/mL of L-ascorbic acid. HAECs were transfected with specific small interfering RNA of PCSK9 (si-PCSK9), and the mRNA and protein expression levels of PCSK9 in HAECs were detected by real-time quantitative PCR and Western blotting. HAECs were randomized into blank group, EndoMT group, EndoMT group transfected with negative control small interfering RNA (si-NC), and EndoMT group transfected with si-PCSK9. The mRNA levels of α-smooth muscle actin (α-SMA), fibroblast-specific protein 1 (FSP1), and vascular endothelial cadherin (VE-cadherin) were detected by real-time quantitative PCR, the protein levels of α-SMA and VE-cadherin were detected by Western blotting, and the expression of α-SMA was detected by immunofluorescence staining. Results 30 mmol/L of β glycerophosphate had the best effect in inducing EndoMT, and the expression of PCSK9 mRNA and protein was up-regulated when EndoMT occurred. After PCSK9 knockdown, the expressions of α-SMA and FSP1 were down-regulated, while the expression of VE cadherin was up-regulated. Conclusion Knockdown of PCSK9 inhibits the EndoMT of HAECs.