血管过氧化物酶1在Ang-Ⅱ诱导血管平滑肌细胞表型转化中的作用及机制

The role and mechanism of vascular peroxidase 1 in Ang-Ⅱ-induced vascular smooth muscle cell phenotype transformation

血管平滑肌细胞(VSMCs)表型转化在动脉粥样硬化等血管增生性疾病中起重要作用,但具体调节机制仍不明确。为探讨血管过氧化物酶1(VPO1)在血管紧张素Ⅱ(Ang-Ⅱ)诱导VSMCs表型转化中的作用及机制,予以Ang-Ⅱ培养VSMCs,结果发现Ang-Ⅱ升高VSMCs内VPO1的表达,伴随着SM22α、α-SMA表达下降和OPN、KLF4表达升高。VPO1基因沉默后可明显抑制Ang-Ⅱ诱导的SM22α、α-SMA表达下降和OPN、KLF4表达升高,同时抑制HOCl的生成。HOCl培养VSMCs使SM22α、α-SMA表达下降和OPN、KLF4表达升高。研究结果表明VPO1通过调节KLF4的表达在Ang-Ⅱ诱导VSMCs表型转化中起重要作用。

Vascular smooth muscle cells(VSMCs)phenotype transformation plays an important role in various vascular proliferative diseases such as atherosclerosis,while the regulation mechanism of VSMCs phenotype transformation remains unclear.To explore the role and mechanism of vascular peroxidase 1(VPO1)in Ang-Ⅱinduced VSMCs phenotype transformation,VSMCs were incubated with Ang-Ⅱand it found that Ang-Ⅱincreased the expression of VPO1 in VSMCs,accompanied by decreased expression of SM22α,α-SMA and elevated expression of OPN and KLF4.The silencing of VPO1 could obviously inhibit the decrease of SM22αandα-SMA induced by Ang-Ⅱ,the increase of OPN and KLF4 expression while the inhibition of HOCl production.HOCl cultured VSMCs that decreased the expression of SM22α,α-SMA and elevated expression of OPN and KLF4.The results showed that VPO1 plays a significant role in Ang-Ⅱinduced VSMCs phenotype transformation through regulating KLF4 protein expression.