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机构地区:[1]中国医科大学附属第一医院,110001 [2]中国医科大学
出 处:《山西医药杂志(上半月)》2009年第7期587-589,共3页Shanxi Medical Journal
基 金:辽宁省自然科学基金(20082092)
摘 要:目的探讨纤维连接蛋白(FN)诱导人胚肺成纤维细胞(HFL-1)增殖的信号转导通路。方法采用不同浓度FN刺激HFL-1并观察磷酸酰基醇-3-激酶(PI3K)信号转导通路抑制剂wortmannin(WMN)、细胞外信号调节蛋白激酶(ERK)信号转导通路抑制剂PD98059和P38蛋白激酶信号转导通路抑制剂SB203580对FN诱导HFL-1增殖作用的影响。用四甲基偶氮唑蓝(MTT)法检测各组细胞增殖情况。结果FN对HFL-1诱导增殖作用呈剂量依赖性升高趋势,在50ng/mL时作用显著;WMN,PD98059和SB203580均可抑制FN诱导的HFL-1细胞增殖。结论FN诱导HFL-1的细胞增殖可以通过PI3K和丝裂原活化蛋白激酶(MAPK)信号转导途径实现。Objective To investigate the signal transduction pathway induced by fibronectin(FN) in human embryonic lung fibroblasts (HFL-1). Methods To stimulate the HFL-1 with different concentrations of FN, and to use phosphatidylinositol 3 kinase (PI3K) signal transduction pathway inhibitor wortmannin(WMN), extraeellular signal regulated protein kinase (ERK) signal transduction pathway inhibitor PD98059 and P38MAPK signal transduction pathway inhibitor SB203580 to check the effects of them on FN induced cell growth. The growth rate of cells was detected by MTT assay. Results The results showed that FN enhanced the HFL-1 proliferation in a dosedependent manner. The effect of FN on the proliferation of HFL-1 was.significant at 50 ng/mL concentration. Proliferation of HFL-1 induced by FN was suppressed by WMN, PD98059 and SB203580. Conclusion The proliferation of HFL-1 induced by FN may be through the PI3K and MAPK signal transduction pathways.
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