目的研究睾酮对氧化型低密度脂蛋白(ox-LDL)诱导大鼠血管平滑肌细胞(VSMC)表型转化和增殖的抑制作用,并探讨其可能机制。方法培养大鼠VSMC,利用血清饥饿法进行同步化处理。将细胞分为对照组:不进行任何处理;ox-LDL组:给予50μg/m L ox-...目的研究睾酮对氧化型低密度脂蛋白(ox-LDL)诱导大鼠血管平滑肌细胞(VSMC)表型转化和增殖的抑制作用,并探讨其可能机制。方法培养大鼠VSMC,利用血清饥饿法进行同步化处理。将细胞分为对照组:不进行任何处理;ox-LDL组:给予50μg/m L ox-LDL处理;睾酮组:分别加入5×10-8mol/L和5×10-7mol/L睾酮预处理12 h,然后与50μg/m L ox-LDL共培养;另外设置血清组,用含100 m L/L胎牛血清的培养基培养。水溶性四甲基偶氮唑盐(WST-1)法检测各组细胞增殖的变化;流式细胞术检测各组细胞周期的变化;Western blot法检测各组细胞线粒体融合素2(Mfn2)、磷酸化的细胞外信号调节激酶1/2(p-ERK1/2)、增殖细胞核抗原(PCNA)、α-平滑肌肌动蛋白(α-SMA)及骨桥蛋白(OPN)表达的变化。结果与对照组比较,ox-LDL组细胞增殖能力增强,G0/G1期细胞比例降低,S期细胞比例增加,Mfn2表达降低,p-ERK1/2表达增加,PCNA表达增加,α-SMA表达降低,OPN表达增加。与ox-LDL组比较,不同浓度睾酮组细胞增殖受抑制,G0/G1期细胞比例增加,S期细胞比例降低,Mfn2表达增加,p-ERK1/2表达降低,PCNA表达降低,α-SMA表达增加,OPN表达降低,以上作用呈现一定的浓度依赖性。结论睾酮可抑制ox-LDL诱导的大鼠VSMC发生表型转化及增殖,可能与其上调Mfn2抑制ERK1/2信号通路有关。展开更多
Lysophosphatidic acid(LPA) is a sort of phospholipid messenger possessing diverse physiological role,which is mediated by its G protein-coupled receptors,and plays a significant role in vascular diseases.Phenotypic mo...Lysophosphatidic acid(LPA) is a sort of phospholipid messenger possessing diverse physiological role,which is mediated by its G protein-coupled receptors,and plays a significant role in vascular diseases.Phenotypic modulation of vascular smooth muscle cells(VSMCs) is the key initiation step of VSMCs proliferation and migration in hypertension,atherosclerosis and postangioplasty restenosis,and is the common morbility foundation of these vascular diseases.In this article we briefly review the LPA biological characteristics,its relationship with VSMCs phenotypic modulation and relative signal transduction pathway.展开更多
文摘目的研究睾酮对氧化型低密度脂蛋白(ox-LDL)诱导大鼠血管平滑肌细胞(VSMC)表型转化和增殖的抑制作用,并探讨其可能机制。方法培养大鼠VSMC,利用血清饥饿法进行同步化处理。将细胞分为对照组:不进行任何处理;ox-LDL组:给予50μg/m L ox-LDL处理;睾酮组:分别加入5×10-8mol/L和5×10-7mol/L睾酮预处理12 h,然后与50μg/m L ox-LDL共培养;另外设置血清组,用含100 m L/L胎牛血清的培养基培养。水溶性四甲基偶氮唑盐(WST-1)法检测各组细胞增殖的变化;流式细胞术检测各组细胞周期的变化;Western blot法检测各组细胞线粒体融合素2(Mfn2)、磷酸化的细胞外信号调节激酶1/2(p-ERK1/2)、增殖细胞核抗原(PCNA)、α-平滑肌肌动蛋白(α-SMA)及骨桥蛋白(OPN)表达的变化。结果与对照组比较,ox-LDL组细胞增殖能力增强,G0/G1期细胞比例降低,S期细胞比例增加,Mfn2表达降低,p-ERK1/2表达增加,PCNA表达增加,α-SMA表达降低,OPN表达增加。与ox-LDL组比较,不同浓度睾酮组细胞增殖受抑制,G0/G1期细胞比例增加,S期细胞比例降低,Mfn2表达增加,p-ERK1/2表达降低,PCNA表达降低,α-SMA表达增加,OPN表达降低,以上作用呈现一定的浓度依赖性。结论睾酮可抑制ox-LDL诱导的大鼠VSMC发生表型转化及增殖,可能与其上调Mfn2抑制ERK1/2信号通路有关。
文摘Lysophosphatidic acid(LPA) is a sort of phospholipid messenger possessing diverse physiological role,which is mediated by its G protein-coupled receptors,and plays a significant role in vascular diseases.Phenotypic modulation of vascular smooth muscle cells(VSMCs) is the key initiation step of VSMCs proliferation and migration in hypertension,atherosclerosis and postangioplasty restenosis,and is the common morbility foundation of these vascular diseases.In this article we briefly review the LPA biological characteristics,its relationship with VSMCs phenotypic modulation and relative signal transduction pathway.
