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Helicobacter pylori ‐downregulated tumor necrosis factor receptor‐associated protein 1 mediates apoptosis of human gastric epithelial cells
Author(s) -
Teng Yongsheng,
Liu Xin,
Han Bin,
Ma Qiang,
Liu Yugang,
Kong Hui,
Lv Yipin,
Mao Fangyuan,
Cheng Ping,
Hao Chuanjie,
Yang Shiming,
Zhang Jinyu,
Peng Liusheng,
Zou Quanming,
Zhuang Yuan
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28223
Subject(s) - caga , helicobacter pylori , downregulation and upregulation , apoptosis , western blot , biology , tumor necrosis factor alpha , virulence factor , heat shock protein , microbiology and biotechnology , immunology , gene , virulence , biochemistry , genetics
Heat shock proteins (HSPs) are crucial proteins in maintaining the homeostasis of human gastric epithelial cells. Tumor necrosis factor receptor‐associated protein 1 (TRAP1), a member of the HSP90 family, has been shown to be involved in various crucial physiological processes, particularly against apoptosis. However, the regulation and function of TRAP1 in Helicobacter pylori infection is still unknown. Here, we found that TRAP1 expression was downregulated on human gastric epithelial cells during H. pylori infection by real‐time polymerase chain reaction (PCR) and western blot analysis. Through virulence factors mutant H. pylori strains infection and inhibitors screening, we found that H. pylori vacuolating cytotoxin A ( vacA ), but not cytotoxin‐associated gene A ( cagA ) protein, induced human gastric epithelial cells to downregulate TRAP1 via P38MAPK pathway by real‐time PCR and western blot analysis. Furthermore, downregulation of TRAP1 with lentivirus carrying TRAP1 short hairpin RNA constructs impairs mitochondrial function, and increases apoptosis of gastric epithelial cells. The results indicate that H. pylori vacA downregulated TRAP1 is involved in the regulation of gastric epithelial cell apoptosis.