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作 者:张丽娟[1] 李倩[1] 陈萍[1] 闫静波[1] 王瑞敏[1] 杨嫣[2] 杨方[1]
机构地区:[1]华北煤炭医学院实验研究中心,唐山063000 [2]北京大学医学部,临床03级北京100083
出 处:《解剖学杂志》2007年第4期416-419,共4页Chinese Journal of Anatomy
基 金:河北省科技厅博士基金(04547002D-5);唐山市新药基础研究重点实验室项目(04362001B-9)
摘 要:目的:探讨血小板衍生生长因子(PDGF)是否通过细胞外信号调节激酶1/2(ERK1/2)途径调节大鼠心脏成纤维细胞增殖和胶原的合成。方法:建立新生大鼠心脏成纤维细胞系,MTT法检测心脏成纤维细胞代谢活性的改变,流式细胞仪法检测细胞周期变化,免疫细胞化学法检测Ⅰ、Ⅲ型胶原表达的改变,Western印迹法检测ERK1/2及Phospho-ERK1/2表达的改变。结果:在PDGF刺激下,大鼠心脏成纤维细胞代谢活性增强,细胞增殖指数(PI)增加,Ⅰ、Ⅲ型胶原表达增加,ERK1/2表达无明显改变,而Phospho-ERK1/2表达增强;25μmol/LPD98059预孵育1h抑制PDGF的以上刺激作用。结论:PDGF能够通过ERK1/2途径调节大鼠心脏成纤维细胞的增殖和胶原合成。Objective: To investigate whether PDGF induces proliferation and collagen synthesis in rat cardiac fibroblasts (CFb) by extracellular signal-regulated klnase 1/2 (ERK 1/2) activation. Methods: Neonatal rat cardiac fibroblasts were isolated. Metabolic activity was observed by MTT. Cell cycle was detected by flow cytometry. Expressions of typeⅠ and type Ⅲcollagen were measured by immunocytochemistry and expressions of phospho-ERK 1/2 and ERK 1/2 were detected by Western blot. Results:Compared with the control group, PDGF increased metabolic activi- ty, proliferous index (PI), expressions of type Ⅰand type Ⅲcollagen and phosphorylation of ERK 1/2, while expressions of ERK 1/2 were not changed. However, PD98059 inhibited these stimulations of PDGF. Conclusion: ERK 1/2 pathway is involved in PDGF-induced proliferation and collagen synthesis of cultured rat cardiac fibroblasts.
关 键 词:细胞外信号调节激酶1/2 血小板衍生生长因子 心 成纤维细胞 细胞增殖 胶原
分 类 号:R54[医药卫生—心血管疾病]
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