Activation of nuclear factor-κB pathway is responsible for tumor necrosis factor-a-induced up-regulation of endothelin B2 receptor expression in vascular smooth muscle cells in vitro

被引:15
|
作者
Zhang, Wei [1 ,2 ]
Li, Xue-Jun [1 ]
Zeng, Xin [1 ]
Shen, Dong-Yan [2 ]
Liu, Chang-Qin [1 ]
Zhang, Hui-Jie [1 ]
Xu, Cang-Bao [1 ,3 ]
Li, Xiao-Ying [1 ,4 ]
机构
[1] Xiamen Diabet Inst, Xiamen 361003, Peoples R China
[2] Xiamen Univ, Affiliated Hosp 1, Ctr Lab, Xiamen 361003, Peoples R China
[3] Lund Univ, Inst Clin Sci Lund, Div Expt Vasc Res, SE-22184 Lund, Sweden
[4] Shanghai Jiao Tong Univ, Sch Med, Rui Jin Hosp, Shanghai Inst Endocrinol & Metab, Shanghai 200025, Peoples R China
基金
中国国家自然科学基金;
关键词
Tumor necrosis factor-alpha; Endothelin B2 receptor; Nuclear factor-kappa B; Vascular smooth muscle cell; SOLUBLE SMOKE PARTICLES; ETB RECEPTORS; FACTOR-ALPHA; PROLIFERATION; CLONING;
D O I
10.1016/j.toxlet.2011.12.005
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The endothelin B2 (ETB2) receptors are induced in vascular smooth muscle cells (VSMCs) in cardiovascular diseases. We tested if in vitro short-term exposure to the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) could up-regulate ETB2 receptors in rat mesenteric arteries, and if this effect is through activation of intracellular nuclear factor-kappa B (NF-kappa B) pathway. The mesenteric arteries were dissected from male Sprague-Dawley rats and the endothelium was removed. The arteries were co-incubated with TNF-alpha in serum-free Dulbecco's modified Eagle's medium. Real-time reverse transcription-PCR, Western blot and immunohistochemical staining were employed to assess the mRNA/protein expression of ETB2 receptors and activation of NF-kappa B pathway. The results showed that, during organ culture. TNF-alpha concentration-dependently enhanced ET52 receptors expression at both mRNA and protein levels, paralleled with activation of NF-kappa B pathway in VSMC. The up-regulated ETB2 receptor expression and NF-kappa B activation could be effectively suppressed by general transcriptional inhibitor actinomycin D, or either of the selective I kappa B kinase inhibitors wedelolactone and IMD-0354. Conclusively, the activation of intracellular NF-kappa B pathway is responsible for the up-regulation of ETB2 receptors induced by short-term exposure to TNF-alpha. This could partly explain the toxic effects of TNF-alpha on VSMCs that account for cardiovascular diseases. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:107 / 112
页数:6
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