The proteomics analysis of extracellular vesicles revealed the possible function of heat shock protein 60 in Helicobacter pylori infection.

The proteomics analysis of extracellular vesicles revealed the possible function of heat shock protein 60 in Helicobacter pylori infection.
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对幽门螺杆菌胞外囊泡的蛋白质组学分析揭示了热休克蛋白60在幽门螺杆菌感染中的可能功能。

DOI:
10.1186/s12935-023-03131-1
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发表时间:
2023-11-16
影响因子:
5.8
通讯作者:
Zhu, Hong
Zhu, Hong
中科院分区:
医学2区
文献类型:
--
作者:
Li, Yujie;Cao, Hui;Qiu, Dewen;Wang, Nan;Wang, Yan;Wen, Tingting;Wang, Jianjun;Zhu, Hong

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幽门螺杆菌(H.幽门螺杆菌)感染是导致胃病(包括胃炎和胃癌)的主要危险因素。热休克蛋白60(HSP 60)是一种参与多种细胞过程的分子伴侣蛋白,与细菌感染的免疫应答有关。细胞外囊泡(extracellular vesicles,EVs)是细胞间通讯的重要组成部分。本研究对从H.进行了pylori感染细胞的实验,并研究了EV衍生的HSP 60功能。通过纳米颗粒跟踪分析、透射电子显微镜和蛋白质印迹法评估EV。通过无标记蛋白质组学对识别的蛋白质组分进行定量,并进行生物信息学分析。HSP 60在H. pylori的检测分别采用免疫印迹法和免疫组化法。此外,还对HSP 60在H. pylori感染情况采用免疫印迹法和流式细胞术进行分析。共鉴定出120个重要的差异蛋白。pylori感染的细胞,并进行基因本体分析。其中CD 63、HSP-70和TSG 101通过蛋白质印迹法进行验证。HSP 60在H.幽门感染的GES-1细胞。H. pylori感染可促进GES-1细胞、AGS细胞、胃粘膜及胃癌组织中HSP 60表达异常增高。此外,HSP 60基因敲低抑制了感染细胞的凋亡和Bcl 2的表达,促进了Bax的上调。这项研究提供了一个全面的蛋白质组学的EV从H。pylori感染的细胞,揭示了HSP 60在H.幽门感染这些发现强调了EV源性HSP 60在H.幽门相关疾病在线版本包含补充材料,可通过10.1186/s12935-023-03131-1获得。
Helicobacter pylori (H. pylori) infection is a major risk factor for gastric diseases, including gastritis and gastric cancer. Heat shock protein 60 (HSP60) is a chaperone protein involved in various cellular processes and has been implicated in the immune response to bacterial infections. Extracellular vesicles (EVs) containing various protein components play important roles in cell communication. In the present study, a systematic proteomic analysis of EVs obtained from H. pylori infected cells was performed and the EV-derived HSP60 function was studied. EVs were evaluated by nanoparticle tracking analysis, transmission electron microscopy and western blotting. The recognized protein components were quantified by label-free proteomics and subjected to bioinformatics assays. The expression of HSP60 in EVs, host cells and gastric cancers infected by H. pylori was determined by western blotting and immunohistochemical, respectively. In addition, the apoptotic regulation mechanisms of HSP60 in H. pylori infection were analyzed by western blotting and flow cytometry. A total of 120 important differential proteins were identified in the EVs from H. pylori-infected cells and subjected to Gene Ontology analysis. Among them, CD63, HSP-70 and TSG101 were verified via western blotting. Moreover, HSP60 expression was significantly increased in the EVs from H. pylori-infected GES-1 cells. H. pylori infection promoted an abnormal increase in HSP60 expression in GES-1 cells, AGS cells, gastric mucosa and gastric cancer. In addition, knockdown of HSP60 suppressed the apoptosis of infected cells and the expression of Bcl2, and promoted the upregulation of Bax. This study provides a comprehensive proteomic profile of EVs from H. pylori-infected cells, shedding light on the potential role of HSP60 in H. pylori infection. The findings underscore the significance of EV-derived HSP60 in the pathophysiology of H. pylori-associated diseases. The online version contains supplementary material available at 10.1186/s12935-023-03131-1.
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发表时间: 2021
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DOI: 10.1073/pnas.1014194107
发表时间: 2010-11-23
影响因子: 11.1
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发表时间: 2019-01-01
影响因子: 0.7
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DOI: 10.3390/ijms22094823
发表时间: 2021-05-01
影响因子: 5.6
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