TRPV4对脑血管平滑肌增殖及凋亡的影响

发布时间：2018-03-24 08:08

  本文选题：TRPV　切入点：脑血管平滑肌细胞　出处：《中风与神经疾病杂志》2017年08期

【摘要】：目的探究新型钙离子通道香草醛受体4(transient receptor potential vanilloid receptor,TRPV4)对自发性高血压(spontaneously hypertensive rats,SHR)大鼠脑血管平滑肌增殖及凋亡的影响。方法分离并培养大鼠脑基底动脉平滑肌细胞(basilar arterial smooth muscle cells,BASMCs),采用实时定量聚合酶链式反应(qRT-PCR)及免疫印迹(Western blot)法检测细胞中TRPV4的表达。转染TRPV4 siRNA沉默TRPV4基因,CCK-8检测细胞增殖、流式细胞术检测细胞周期及凋亡;Western blot检测cyclin D1、p-Rb、Bcl-2、cleaved-caspase-3/caspase-3、p-AKT/AKT、p-GSK3β/GSK3β蛋白表达。结果 qRT-PCR及Western blot结果显示自发性高血压大鼠BASMCs中TRPV4的表达明显高于对照组大鼠。而在自发性高血压大鼠BASMCs中,沉默TRPV4可抑制细胞增殖,阻滞细胞周期并诱导其凋亡;此外还可下调cyclin D1、p-Rb、Bcl-2、p-AKT、p-GSK3β蛋白的表达,同时上调cleaved-caspase-3蛋白的表达。结论沉默TRPV4能够抑制自发性高血压大鼠BASMCs细胞增殖,同时促进细胞凋亡,机制可能与抑制AKT/GSK3β信号通路的激活有关,所以新型钙离子通道TRPV4可为今后靶向诊疗高血压脑血管疾病提供依据。
[Abstract]:Objective to investigate the effects of 4(transient receptor potential vanilloid receptor TRPV4, a new calcium channel, on the proliferation and apoptosis of cerebral vascular smooth muscle cells in spontaneously hypertensive hypertensive ratshr rats. Methods basilar arterial smooth was isolated and cultured from rat basilar arterial smooth. The expression of TRPV4 in muscle cells was detected by real-time quantitative polymerase chain reaction and Western blotting. TRPV4 siRNA silencing TRPV4 gene CCK-8 was used to detect cell proliferation. Flow cytometry was used to detect the cell cycle and apoptosis. The expression of TRPV4 in BASMCs of spontaneously hypertensive rats was significantly higher than that of control rats, while the expression of TRPV4 in BASMCs of spontaneously hypertensive rats was significantly higher than that of control rats, and the expression of TRPV4 in BASMCs of spontaneously hypertensive rats was significantly higher than that of control rats, and the expression of TRPV4 in BASMCs of spontaneously hypertensive rats was significantly higher than that of control rats, and the expression of TRPV4 in BASMCs of spontaneously hypertensive rats was significantly higher than that of control rats, and the expression of TRPV4 in BASMCs of spontaneously hypertensive rats was significantly higher than that of control rats. Silencing TRPV4 can inhibit cell proliferation, block cell cycle and induce apoptosis, in addition, it can down-regulate the expression of Bcl-2Bcl-AKTnp-GSK3 尾 protein and up-regulate the expression of cleaved-caspase-3 protein in BASMCs cells of spontaneously hypertensive rats. Conclusion silencing TRPV4 can inhibit the proliferation of BASMCs cells in spontaneously hypertensive rats. The mechanism may be related to the inhibition of activation of AKT/GSK3 尾 signaling pathway. Therefore, a new calcium channel TRPV4 may provide evidence for the future diagnosis and treatment of hypertensive cerebrovascular diseases.
【作者单位】： 新乡医学院第一附属医院神经内五科;
【基金】：河南卫计委项目(201602154)资助
【分类号】：R743
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本文编号：1657436