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激活TRPV1对自发性高血压大鼠血管平滑肌细胞增殖的影响

, PP. 762-766

Keywords: 瞬时受体电位香草醛亚家族,自发性高血压大鼠,血管平滑肌细胞,细胞增殖

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Abstract:

目的探讨瞬时受体电位香草醛亚家族1(transientreceptorpotentialvanilloid1,TRPV1)对培养的血管平滑肌细胞(vascularsmoothmusclecells,VSMCs)增殖的影响。方法用组织贴块法分别培养SHR和WKY大鼠的主动脉VSMCs,采用细胞免疫荧光进行鉴定。分别用辣椒素和iRTX激活和拮抗TRPV1受体,CCK-8法检测VSMCs增殖;Westernblot法检测TRPV1、磷酸化-Akt(p-Akt)和总Akt(t-Akt)的蛋白表达。结果①SHR-VSMCs中TRPV1蛋白相对表达量低于WKY-VSMCs(0.32±0.05vs0.55±0.11,P<0.05);TRPV1激动剂辣椒素可显著上调SHR-VSMCs(0.65±0.19)和WKY-VSMCs(0.89±0.13)中TRPV1的表达(P<0.05)。②SHR-VSMCs的增殖能力高于WKY-VSMCs(1.30±0.07vs0.88±0.23,P<0.05);辣椒素呈剂量依赖性地抑制SHR-VSMCs的增殖(对照组:1.30±0.07,1μmol/L辣椒素组:0.93±0.10,10μmol/L辣椒素组:0.83±0.16,P<0.05);应用iRTX拮抗TRPV1即拮抗辣椒素的抗增殖作用(1μmol/L辣椒素组:0.93±0.10,1μmol/L辣椒素+1μmol/LiRTX组:1.23±0.14,P<0.05)。③SHR-VSMCs中Akt磷酸化水平高于WKY-VSMCs(0.44±0.02vs0.29±0.09,P<0.05);辣椒素激活TRPV1抑制VSMCs中Akt的磷酸化(WKY-VSMCs:0.13±0.02,SHR-VSMCs:0.23±0.03,P<0.05);TRPV1拮抗剂iRTX可拮抗辣椒素作用,使WKY-VSMCs(0.37±0.07)、SHR-VSMCs(0.43±0.10)中Akt磷酸化水平升高(P<0.05)。结论激活TRPV1可能通过抑制Akt的磷酸化而抑制SHR-VSMCs增殖。

References

[1]  Owens G K, Kumar M S, Wamhoff B R. Molecular regulation of vascular smooth muscle cell differentiation in development and disease [J]. Physiol Rev, 2004, 84(3): 767-801.? [2]Schiffrin E L. Vascular remodeling in hypertension: mechanisms and treatement [J]. Hypertension, 2012, 59(2): 367-374.? [3]Zhu Z, Luo Z, Ma S, et al. TRP channels and their implications in metabolic diseases [J]. Pflugers Arch, 2011, 461(2): 211-223.? [4]Ma L, Zhong J, Zhao Z, et al. Activation of TRPV1 reduces vascular lipid accumulation and attenuates atherosclerosis [J]. Cardiovasc Res, 2011, 92(3): 504-513.? [5]Yang D, Luo Z, Ma S, et al. Activation of TRPV1 by dietary capsaicin improves endothelium-dependent vasorelaxation and prevents hypertension [J]. Cell Metab, 2010, 12(2): 130-141.? [6]Huang W, Rubinstein J, Prieto A R, et al. Transient receptor potential vanilloid gene deletion exacerbates inflammation and atypical cardiac remodeling after myocardial infarction [J]. Hypertension, 2009, 53(2): 243-250.? [7]Xu X, Wang P, Zhao Z, et al. Activation of transient receptor potential vanilloid 1 by dietary capsaicin delays the onset of stroke in stroke-prone spontaneously hypertensive rats [J]. Stroke, 2011, 42(11): 3245-3251.? [8]Savoia C, Burger D, Nishigaki N, et al. Angiotensin II and the vascular phenotype in hypertension [J]. Expert Rev Mol Med, 2011, 13: e11.? [9]Zhang L, Xie P, Wang J, et al. Impaired peroxisome proliferator-activated receptor-gamma contributes to phenotypic modulation of vascular smooth muscle cells during hypertension [J]. J Biol Chem, 2010, 285(18): 13666-13677. [10]Bonta P I, Pols T W, van-Tiel C M, et al. Nuclear receptor Nurr1 is expressed in and is associated with human restenosis and inhibits vascular lesion formation in mice involving inhibition of smooth muscle cell proliferation and inflammation [J]. Circulation, 2010, 121(18): 2023-2032.? [11]皮燕, 张莉莉, 胡子成, 等. miR-145表达状态对大鼠高血压动脉内膜增生的影响[J]. 第三军医大学学报, 2013, 35(8): 707-711.? [12]李魁君, 李春刚, 刘兴君. 辣椒素受体(TRPV1)的生物学作用及其作为药物靶点的研究进展[J]. 沈阳药科大学学报, 2011, 28(11): 917-927.? [13]Wang Q, Ma S, Li D, et al. Dietary capsaicin ameliorates pressure overload-induced cardiac hypertrophy and fibrosis through the transient receptor potential vanilloid type 1[J]. Am J Hypertens, 2014, 27(12): 1521-1529.? [14]Zhang L L, Yan-Liu D, Ma L Q, et al. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity[J]. Circ Res, 2007, 100(7): 1063-1070.? [15]Li B H, Yin Y W, Liu Y, et al. TRPV1 activation impedes foam cell formation by inducing autophagy in oxLDL-treated vascular smooth muscle cells[J]. Cell Death Dis, 2014, 5: e1182.? [16]Choi K H, Kim J E, Song N R, et al. Phosphoinositide 3-kinase is a novel target of piceatannol for inhibiting PDGF-BB-induced proliferation and migration in human aortic smooth muscle cells [J]. Cardiovasc Res, 2010, 85(4): 836-844.? [17]Dai W, Bai Y, Hebda L, et al. Calcium deficiency-induced and TRP channel-regulated IGF-PI3K-Akt signaling regulates abnormal epithelial cell proliferation [J]. Cell Death Differ, 2014, 21(4): 568-581.? [18]Li S, Bode A M, Zhu F, et al. TRPV1-antagonist AMG9810 promotes mouse shin tumorigenesis through EGFR/Akt signaling [J]. Carcinogenesis, 2011, 32(5): 779-785.

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