Airborne fine particulate matter induces an upregulation of endothelin receptors on rat bronchi.
Airborne fine particulate matter induces an upregulation of endothelin receptors on rat bronchi.
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空气中的细颗粒物会诱导大鼠支气管内皮素受体的上调。
DOI：
10.1016/j.envpol.2015.10.043
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发表时间：
2016-02
影响因子：
8.9
通讯作者：
Yong-Xiao Cao
中科院分区：
文献类型：
--
作者：
Lei Cao;Zhen-Xing Shen;Ying Lei;Yong-Xiao Cao
空气中的细颗粒物(PM2.5)是呼吸系统疾病的危险因素。然而，人们对PM2.5对支气管的影响知之甚少。本研究探讨了空气中PM2.5对大鼠支气管的影响及其机制。分离的大鼠支气管段培养24小时后，用钢丝肌图仪记录内皮素(ET)受体介导的收缩反应。用实时定量聚合酶链式反应、Western blotting和免疫组织化学方法检测ET受体的mRNA和蛋白表达水平。结果表明，ETA和ETB受体激动剂对新鲜和培养的支气管段均有明显的收缩反应。PM2.5(1.0或3.0μg/ml)显著增强ETA和ETB受体介导的支气管收缩反应，最大收缩幅度明显高于二甲基亚砜或Fresh组。PM2.5使ETA和ETB受体的mRNA和蛋白表达水平升高。U0126(MEK1/2抑制剂)和SB203580(p38抑制剂)显著抑制PM2.5诱导的ETB受体介导的收缩反应、mRNA和蛋白水平的增加。SP600125(JNK抑制剂)和SB203580可显著抑制PM2.5诱导的ETA受体介导的收缩和受体表达的增强。总而言之，PM2.5上调了支气管中的ET受体。ETB受体上调与MEK1/2和p38途径有关，而ETA受体上调与JNK和p38途径有关。
Airborne fine particulate matter (PM2.5) is a risk factor for respiratory diseases. However, little is known about the effects of PM2.5 on bronchi. The present study investigated the effect of airborne PM2.5 on rat bronchi and the underlying mechanisms. Isolated rat bronchial segments were cultured for 24 h. Endothelin (ET) receptor-mediated contractile responses were recorded using a wire myograph. The mRNA and protein expression levels of ET receptors were studied using quantitative real-time PCR, Western blotting, and immunohistochemistry. The results demonstrated that ETAand ETBreceptor agonists induced remarkable contractile responses on fresh and cultured bronchial segments. PM2.5 (1.0 or 3.0 μg/ml) significantly enhanced ETAand ETBreceptor-mediated contractile responses in bronchi with a markedly increased maximal contraction compared to the DMSO or fresh groups. PM2.5 increased the mRNA and protein expression levels of ETAand ETBreceptors. U0126 (a MEK1/2 inhibitor) and SB203580 (a p38 inhibitor) significantly suppressed PM2.5-induced increases in ETBreceptor-mediated contractile responses, mRNA and protein levels. SP600125 (a JNK inhibitor) and SB203580 significantly abrogated the PM2.5-induced enhancement of ETAreceptor-mediated contraction and receptor expression. In conclusion, PM2.5 upregulates ET receptors in bronchi. ETBreceptor upregulation is associated with MEK1/2 and p38 pathways, and the upregulation of ETAreceptor is involved in JNK and p38 pathways.
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影响因子：
--
作者：
Cang-bao Xu;P. Vikman;T. Krag;L. Edvinsson
通讯作者：
Cang-bao Xu;P. Vikman;T. Krag;L. Edvinsson
DOI：
10.1016/s0091-6749(96)70076-3
发表时间：
1996-12
期刊：
The Journal of allergy and clinical immunology
影响因子：
--
作者：
Stephen I. Rennard
通讯作者：
Stephen I. Rennard
吸烟颗粒通过增强大鼠支气管中的翻译来增强内皮素A和内皮素B受体介导的收缩。
影响因子：
3.1
作者：
Granstrom, Bengt W;Xu, Cang-Bao;Nilsson, Elisabeth;Vikman, Petter;Edvinsson, Lars
通讯作者：
Edvinsson, Lars
影响因子：
7.3
作者：
L. Fernandes;P. Henry;P. Rigby;R. Goldie
通讯作者：
L. Fernandes;P. Henry;P. Rigby;R. Goldie
影响因子：
4.4
作者：
M. S. Haque;T. Taniguchi;K. Sugiyama;K. Okada;Y. Kitazawa
通讯作者：
M. S. Haque;T. Taniguchi;K. Sugiyama;K. Okada;Y. Kitazawa