本文選題：TRPV　切入點(diǎn)：腦血管平滑肌細(xì)胞　出處：《中風(fēng)與神經(jīng)疾病雜志》2017年08期

【摘要】：目的探究新型鈣離子通道香草醛受體4(transient receptor potential vanilloid receptor,TRPV4)對(duì)自發(fā)性高血壓(spontaneously hypertensive rats,SHR)大鼠腦血管平滑肌增殖及凋亡的影響。方法分離并培養(yǎng)大鼠腦基底動(dòng)脈平滑肌細(xì)胞(basilar arterial smooth muscle cells,BASMCs),采用實(shí)時(shí)定量聚合酶鏈?zhǔn)椒磻?yīng)(qRT-PCR)及免疫印跡(Western blot)法檢測(cè)細(xì)胞中TRPV4的表達(dá)。轉(zhuǎn)染TRPV4 siRNA沉默TRPV4基因,CCK-8檢測(cè)細(xì)胞增殖、流式細(xì)胞術(shù)檢測(cè)細(xì)胞周期及凋亡;Western blot檢測(cè)cyclin D1、p-Rb、Bcl-2、cleaved-caspase-3/caspase-3、p-AKT/AKT、p-GSK3β/GSK3β蛋白表達(dá)。結(jié)果 qRT-PCR及Western blot結(jié)果顯示自發(fā)性高血壓大鼠BASMCs中TRPV4的表達(dá)明顯高于對(duì)照組大鼠。而在自發(fā)性高血壓大鼠BASMCs中,沉默TRPV4可抑制細(xì)胞增殖,阻滯細(xì)胞周期并誘導(dǎo)其凋亡;此外還可下調(diào)cyclin D1、p-Rb、Bcl-2、p-AKT、p-GSK3β蛋白的表達(dá),同時(shí)上調(diào)cleaved-caspase-3蛋白的表達(dá)。結(jié)論沉默TRPV4能夠抑制自發(fā)性高血壓大鼠BASMCs細(xì)胞增殖,同時(shí)促進(jìn)細(xì)胞凋亡,機(jī)制可能與抑制AKT/GSK3β信號(hào)通路的激活有關(guān),所以新型鈣離子通道TRPV4可為今后靶向診療高血壓腦血管疾病提供依據(jù)。
[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.
【作者單位】： 新鄉(xiāng)醫(yī)學(xué)院第一附屬醫(yī)院神經(jīng)內(nèi)五科;
【基金】：河南衛(wèi)計(jì)委項(xiàng)目(201602154)資助
【分類號(hào)】：R743
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本文編號(hào)：1657436