Involvement of water channel Aquaporin 5 in H2S-induced pulmonary edema.
Involvement of water channel Aquaporin 5 in H2S-induced pulmonary edema.
复制标题
水通道水通道蛋白 5 参与 H2S 诱导的肺水肿。
DOI：
10.1016/j.etap.2016.12.013
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Zhu B;Zhang H;Wang J;Zhang J
硫化氢（H2S）急性暴露对生命构成重大威胁，肺是H2S的主要靶器官之一。然而，参与H2S诱导的急性肺水肿的机制知之甚少。本研究旨在探讨硫化氢对水通道蛋白5（AQP 5）表达的影响，并阐明参与AQP 5调控的信号通路。在体内实验中，采用亚致死浓度H_2S吸入染毒C57 BL 6小鼠，观察其肺组织学损伤和肺上皮细胞超微结构损伤。通过实时荧光定量PCR和Western blot分析，我们发现H2S暴露导致小鼠肺组织和A549细胞系中AQP 5表达显著降低，并且ERK 1/2和p38 MAPK信号通路被证明参与AQP 5的调节。因此，调节AQP 5蛋白水平可以被认为是治疗H2S和其他有害气体诱导的APE的治疗策略。
Acute exposure to hydrogen sulfide (H2S) poses a significant threat to life, and the lung is one of the primary target organs of H2S. However, the mechanisms involved in H2S-induced acute pulmonary edema are poorly understood. This study aims to investigate the effects of H2S on the expression of water channel aquaporin 5 (AQP5) and to elucidate the signaling pathways involved in AQP5 regulation. In anin vivostudy, C57BL6 mice were exposed to sub-lethal concentrations of inhaled H2S, and histological injury of the lungs and ultrastructure injury of the epithelial cells were evaluated. With real-time PCR and western blot assays, we found that H2S exposure contributed to a significant decrease in AQP5 expression both in murine lung tissue and the A549 cell line, and the ERK1/2 and p38 MAPK signaling pathways were demonstrated to be implicated in AQP5 regulation. Therefore, adjusting AQP5 protein levels could be considered a therapeutic strategy for the treatment of APE induced by H2S and other hazardous gases.
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水通道蛋白5的缺失会加重铜绿假单胞菌引起的急性肺损伤。
DOI：
10.1097/ta.0b013e3182128528
发表时间：
2011-11
期刊：
The Journal of trauma, injury, infection, and critical care
影响因子：
--
作者：
Bai CX;Zhang ZQ;Song YL
通讯作者：
Song YL
影响因子：
7.7
作者：
Chen, Hai-hua;Zhou, Xian-long;Yang, Jiong
通讯作者：
Yang, Jiong
影响因子：
3.4
作者：
Moore, M;Ma, TH;Verkman, AS
通讯作者：
Verkman, AS
影响因子：
3.2
作者：
Jin, Yingyu;Yu, Guangzhe;Xin, Xiaomin
通讯作者：
Xin, Xiaomin
影响因子：
3.7
作者：
Wang J;Zhang H;Su C;Chen J;Zhu B;Zhang H;Xiao H;Zhang J
通讯作者：
Zhang J