摘要:目的: 探討在血管緊張素Ⅱ(AngⅡ)誘導血管平滑肌細胞(VSMCs)NOX1基因表達增加中線粒體所起的作用。 方法 :體外培養大鼠主動脈VSMCs,用線粒體呼吸鏈的抑制劑阻斷線粒體的作用,用熒光實時定量PCR檢測NOX1基因表達的量。 結果 :AngⅡ能夠誘導 NOX1基因的表達增加,線粒體呼吸鏈的抑制劑能夠抑制上述這一作用。 結論 :在大鼠的VSMCs中,AngⅡ誘導NOX1的增加通過線粒體呼吸的作用。Abstract: Objective: To detect the role of mitochondria involved in Angiotensin Ⅱ(Ang Ⅱ) induced NOX1 gene expression. Methods :Rat aortic vascellum smooth muscle cells(VSMCs) were cultured in vitro,and were treated with or without some inhibitors of complexs in mitochondrial respiratory chain. Realtime RTPCR was used to calculate the expression of NOX1 mRNA. Results :AngⅡ stimulated NOX1 gene expression,while some inhibitors of complexs in mitochondrial respiratory chain attenuated this progress.〖WTHZ〗Conclusion : Mitochondrial respiratory chain mediates expression of NOX1 gene in VSMCs by AngⅡ.
摘要:目的: 探討激活轉錄因子(ATF1)在血管緊張素Ⅱ(AngⅡ)誘導血管平滑肌細胞(VSMCs)中NOX1基因表達增加的作用。 方法 :體外培養大鼠主動脈VSMCs,用熒光實時定量逆轉錄PCR(Realtime RTPCR)檢測NOX1基因表達的量,Western Blot檢測ATF1蛋白在AngⅡ的刺激是否引起NOX1基因的高表達并用RNA干擾(RNAi)技術轉染VSMCs使ATF1基因沉默來觀察NOX1的表達。 結果 :AngⅡ能夠誘導 NOX1基因的表達增加以及增強ATF1的磷酸化及活性,ATF1基因沉默反過來可抑制AngⅡ誘導的NOX1基因表達的增加。 結論 :在大鼠的VSMCs中,ATF1是介導NOX1基因表達的一個必須的轉錄因子。Abstract: Objective: To detect the role of activating transcription factor (ATF1) involved in angiotensinⅡ(AngⅡ) stimulated NOX1 gene expression.Methods :Rat aortic vascellum smooth muscle cells(VSMCs) were cultured in vitro.Use Realtime RTPCR to measure the expression of NOX1 gene.Western Blot Analysis was carried out to test the activity of ATF1 protein. RNA interference was used and transfected into VSMCs to knockdown ATF1 gene expression, and then measured NOX1 gene expression.Results : AngⅡ stimulated NOX1 gene expression and phosphorylation of ATF1 Gene silencing of ATF1 attenuated the upregulation of NOX1 mRNA by AngⅡ. Conclusion :ATF1 is an essential transcription factor that mediates expression of NOX1 gene in VSMCs by AngⅡ.
