Autor: |
Pei, Wang, Wei, Zhao, Jie, Sun, Tao, Tao, Xin, Chen, Yan-Yan, Zheng, Cheng-Hai, Zhang, Zhong, Chen, Yun-Qian, Gao, Fan, She, Ye-Qiong, Li, Li-Sha, Wei, Ping, Lu, Cai-Ping, Chen, Ji, Zhou, Da-Quan, Wang, Liang, Chen, Xiao-Hao, Shi, Linhong, Deng, Ronghua, ZhuGe, Hua-Qun, Chen, Min-Sheng, Zhu |
Rok vydání: |
2017 |
Předmět: |
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Zdroj: |
The Journal of allergy and clinical immunology. 141(4) |
ISSN: |
1097-6825 |
Popis: |
Allergic inflammation has long been implicated in asthmatic hyperresponsiveness of airway smooth muscle (ASM), but its underlying mechanism remains incompletely understood. Serving as G protein-coupled receptor agonists, several inflammatory mediators can induce membrane depolarization, contract ASM, and augment cholinergic contractile response. We hypothesized that the signal cascade integrating on membrane depolarization by the mediators might involve asthmatic hyperresponsiveness.We sought to investigate the signaling transduction of inflammatory mediators in ASM contraction and assess its contribution in the genesis of hyperresponsiveness.We assessed the capacity of inflammatory mediators to induce depolarization currents by electrophysiological analysis. We analyzed the phenotypes of transmembrane protein 16A (TMEM16A) knockout mice, applied pharmacological reagents, and measured the CaInflammatory mediators, such as 5-hydroxytryptamin, histamine, U46619, and leukotriene DA G protein-coupled receptor-TMEM16A-voltage-dependent Ca |
Databáze: |
OpenAIRE |
Externí odkaz: |
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