钙池操纵的Ca~(2+)通道在IL-13促气道平滑肌细胞增殖中的作用

目的:探讨钙池操纵的Ca2+(SOC)通道在Th2型细胞因子IL-13促进气道平滑肌细胞(ASMCs)增殖中的作用。方法:体外分离培养大鼠ASMCs,IL-13孵育36 h后,以Fluo 3-AM为钙荧光示踪剂,采用激光共聚焦显微镜,测定大鼠ASMCs基础Ca2+水平以及肌浆网钙泵抑制剂Thapsigargin(TPG)诱发的内钙释放和经SOC通道的外钙内流;采用四甲基偶氮唑蓝比色法(MTT法),检测SOC通道阻断剂SKF-96365对IL-13促增殖作用的影响。结果:①IL-13作用36 h后,ASMCs的内钙释放及经SOC通道的钙内流反应明显高于对照组(P<0.05),并且这种钙内流反应能部分被SOC通道阻断剂SKF-96365抑制(P<0.01)。②IL-13能促进气道平滑肌细胞增殖,该作用可被SKF-96365抑制(P<0.01)。结论:IL-13对气道平滑肌细胞的促增殖作用可能部分是通过促进SOC通道钙离子内流反应来实现的。

Role of Store-Operated Ca~(2+) Entry in IL-13-Promoted Proliferation of Airway Smooth Muscle Cells

Objective: To investigate the role of store-operated Ca2+(SOC) entry in the mechanism of IL-13 promoting effects on the proliferation of airway smooth muscle cells(ASMCs).Methods: Rat ASMCs were isolated and subcultured,and then exposed to 20 μg/L IL-13 for 36 hours.Calcium indicator dye fluo 3-AM was used to determine the intracellular calcium concentration in ASMCs with a confocal microscope.The promoting effects of IL-13 on the proliferation of ASMCs were determined by MTT assay.Results: After exposure of ASMCs to 20 μg/L IL-13 for 36 hours,the net Ca2+ releases and influxes were significantly(P<0.05) higher in IL-13-treated ASMCs than controls;the augmented Ca2+ influxes were significantly(P<0.05) attenuated by SOC channel blocker SKF-96365 in IL-13-treated ASMCs.IL-13 promoted the proliferation of ASMCs,and this effect of IL-13 could be inhibited by SKF-96365.Conclusion: IL-13-promoted proliferation of ASMCs is partially mediated by Ca2+ influxes through SOC channels.