【摘要】 目的运用芯片技术研究内源性一氧化碳(CO)刺激下血管平滑肌细胞凋亡相关基因表达谱的变化。方法取Sprague-Dawley(SD)大鼠肺动脉平滑肌细胞进行离体培养,用血小板源性生长因子BB(platelet-de-rived growth factor,PDGF-BB,20ng/mL)和高氯血红素(hemin,20μg/mL)进行刺激后2h,用Affymetrix表达基因谱芯片检测其基因表达谱变化。结果 PDGF刺激后,Map2k3(P38)信号通路中相关差异表达基因Kras、Nras、丝分裂原蛋白激酶的激酶Map2k3、细胞周期素CyclinD1、CyclinH、CyclinL1等的表达显著上调,而周期素依赖性蛋白激酶抑制因子P27的表达显著下调。Hemin刺激后,P53依赖途径中的一些基因如:Gadd45α、P21、Trp53inp1表达显著上调。结论内源性CO所引发的血管平滑肌细胞的凋亡可能与P53调控途径密切相关。更多还原

【Abstract】 Objective To identify the gene expression profiles associated with the apoptosis of pulmonary arterial smooth muscle cells stimulated by carbon monoxide(CO).Methods Primary cultured Sprague-Dawley rat pulmonary arterial smooth muscle cells(PASMC) were stimulated by platelet-derived growth factor(PDGF,20 ng/mL) and hemin(20 μmol/L).Cells were harvested after 2 hrs and Affymetrix microarrays were used to detect the gene expression profile.Results Some genes associated with Map2k3(P38) signal pathway,such as CyclinD1,CyclinH,CyclinL1,MAP2K3,Kras and Nras,were upregulated,but P27 expression was downregulated after PDGF treatment.After endogenous CO treatment,some genes associated with P53 pathway,such as Gadd45α,P21 and Trp53inp1,were upregulated.Conclusions P53 pathway probably plays an important role in apoptosis of pulmonary arterial smooth muscle cells treated with endogenous CO.更多还原