乙二胺四乙酸通过降低[Ca2+]i抑制创伤弧菌诱导的树突细胞凋亡。

Q1 Medicine

Neurosignals Pub Date : 2018-01-01 Epub Date: 2018-05-22 DOI:10.1159/000489951

Ping Qian, Bo Hu, Yuzhang Zhu, Dongliang Shao, Huaifeng Zhang, Huafei Huang, Lizhong Wang, Ruilin Shen

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引用次数: 0

摘要

背景/目的:创伤弧菌(V. vulnificus)是一种革兰氏阴性海洋细菌，可引起危及生命的原发性败血症，特别是在先天免疫系统中。但是创伤弧菌如何影响和作用于树突状细胞(DC)尚不清楚。本研究旨在探讨[Ca2+]i在创伤弧菌B2诱导的DC细胞凋亡中的变化及mTor-STAT3-Bcl-2信号通路的表达，并在创伤弧菌B2和DC2.4细胞共培养感染模型中，以EDTA为干预剂，探讨乙二胺四乙酸(ethylenediaminetetraacetic acid, EDTA)对DC细胞凋亡的保护作用。方法:分别用细胞术、Fluo-8-AM和Western blotting检测细胞凋亡率、[Ca2+]i和STAT3、m-Tor、Bcl-2的表达。结果:EDTA抑制[Ca2+]i的升高，上调m-Tor-STAT3-Bcl-2信号通路的表达，对创伤弧菌b2诱导的DC细胞凋亡具有保护作用。结论:EDTA通过m-Tor-STAT3-Bcl-2信号通路降低[Ca2+]i抑制V. vulnificus诱导的DC细胞凋亡。

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Ethylenediaminetetraacetic Acid Inhibits Vibrio Vulnificus-Induced Dendritic Cell Apoptosis by Lowering [Ca2+]i.

Background/aims: Vibrio vulnificus (V. vulnificus) is a Gram-negative marine bacterium that can cause life-threatening primary septicemia, especially in the innate immune system. But how V. vulnificus affects and acts on dendritic cells (DC) is not well understood. The aim of the present study is to investigate [Ca2+]i change and the expression of the mTor-STAT3-Bcl-2 signaling pathway in V. vulnificus B2-induced DC apoptosis, and explore the protective effect of ethylenediaminetetraacetic acid (EDTA) against DC apoptosis in a V. vulnificus B2 and DC2.4 cell coculture infection model, using EDTA as an intervenient.

Methods: The apoptosis rate, [Ca2+]i, and the expression of STAT3, m-Tor and Bcl-2 were detected by cytometry, Fluo-8-AM and Western blotting respectively.

Results: The results demonstrated that EDTA inhibited the increase of [Ca2+]i, upregulated the expression of m-Tor-STAT3-Bcl-2 signaling pathway, and protected DC against V. vulnificus B2-induced apoptosis.

Conclusions: EDTA inhibits V. Vulnificus-induced DC apoptosis by lowering [Ca2+]i via m-Tor-STAT3-Bcl-2 signaling pathway.

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来源期刊

Neurosignals 医学-神经科学

CiteScore

3.40

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Neurosignals is an international journal dedicated to publishing original articles and reviews in the field of neuronal communication. Novel findings related to signaling molecules, channels and transporters, pathways and networks that are associated with development and function of the nervous system are welcome. The scope of the journal includes genetics, molecular biology, bioinformatics, (patho)physiology, (patho)biochemistry, pharmacology & toxicology, imaging and clinical neurology & psychiatry. Reported observations should significantly advance our understanding of neuronal signaling in health & disease and be presented in a format applicable to an interdisciplinary readership.