胰岛素促进大鼠体外血管平滑肌细胞 RANKL表达
the effects of insulin on the expression of RANKL in rat Vascular smooth muscle cells
目的：探讨胰岛素对大鼠体外钙化型血管平滑肌细胞（CVSMCs） RANKL表达的影响及其细胞信号机制。方法：取不同浓度及时间点，用胰岛素干预大鼠CVSMCs。应用RT-PCR和ELISA方法分别测定CVSMCs RANKL mRNA和RANKL蛋白在大鼠CVSMCs的表达。胰岛素以及联合ERK1/2信号转导阻断剂PI3K信号转导阻断剂和AKt信号转导阻断剂干预大鼠CVSMCs，利用Western Blot 检测p-ERK1/2，ERK1/2，p-Akt，Akt的表达情况。胰岛素以及联合ERK1/2信号转导阻断剂PD98509、PI3K信号转导阻断剂LY294002和AKt信号转导阻断剂HIMO干预大鼠CVSMCs，利用RT-PCR技术检测RANKL mRNA 表达水平。结果：1.胰岛素促进CVSMCs RANKL mRNA和RANKL蛋白的表达。2.胰岛素呈时间依赖性促进CVSMCs RANKL mRNA表达。3.胰岛素诱导大鼠CVSMCs ERK1/2以及Akt磷酸化。4.ERK1/2信号转导阻断剂PD98509干预组抑制胰岛素促进大鼠CVSMCs RANKL mRNA表达增加效应，而PI3K信号转导阻断剂LY294002组和AKt信号转导阻断剂HIMO组无该抑制效应。结论：胰岛素通过激活ERK1/2信号转导途径促进大鼠CVSMCs RANKL表达。
Objective，To investigate the effects and the signal pathway invovled in insulin-induced RANKL expression in rat CVSMCs. Methods：The expression of RANKL mRNA in CVSMCs was detected by RT-PCR and RANKL protein was analyzed by ELISA. Insulin, PD98059 (an inhibitor of ERK 1/2), LY294002 (an inhibitor of PI3-K) or HIMO (an inhibitor of Akt) treated CVSMCs in vitro, p-ERK1/2, ERK1/2, p-Akt, Akt were analysed by Western blot. The expression of RANKL mRNA in rat VSMCs was detected by RT-PCR. Results: 1.Insulin increased the expression of RANKL mRNA and protein in rat CVSMCs .2. Insulin increased the expression of RANKL mRNA in a time-dependent manner. 3.Insulin induced ERK 1/2 and Akt signal pathway in rat CVSMCs.4.The cffect that insulin increased CVSMCs RANKL mRNA was blocked by pretreatment of CVSMCs with ERK inhibitor.That data suggested that ERK played an important role in increasing the expression of RANKL in rat CVSMCs. Conclusion: Insulin promoted expression of RANKL though ERK 1/2 activation, but not PI3K/Akt activation in rat CVSMCs.
汪化文、朱佳花、周华、刘幼硕、袁凌青、廖二元
基础医学生理学细胞生物学
胰岛素钙化型血管平滑肌细胞RANKL
InsulinCVSMCsRANKL
汪化文,朱佳花,周华,刘幼硕,袁凌青,廖二元.胰岛素促进大鼠体外血管平滑肌细胞 RANKL表达[EB/OL].(2012-01-16)[2025-07-16].http://www.paper.edu.cn/releasepaper/content/201201-519.点此复制
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