Macrophages-derived high-mobility group box-1 protein induces endothelial progenitor cells pyroptosis

被引:1
作者
Zeng, Menghao [1 ,2 ]
Liang, Guibin [1 ,2 ]
Yuan, Fangfang [1 ]
Yan, Shanshan [1 ]
Liu, Jie [1 ]
He, Zhihui [1 ,2 ,3 ]
机构
[1] Cent South Univ, Xiangya Hosp 3, Dept Crit Care Med, Changsha 410013, Hunan, Peoples R China
[2] Sepsis Translat Med Key Lab Hunan Prov, Changsha, Hunan, Peoples R China
[3] Natl Engn Res Ctr Human Stem Cells, Changsha, Hunan, Peoples R China
基金
中国国家自然科学基金;
关键词
GASDERMIN D; HMGB1; INFLAMMATION; SEPSIS; RAGE; MECHANISM; CASPASES; CLEAVAGE; DEATH; GSDMD;
D O I
10.1016/j.isci.2024.110996
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Endothelial dysfunction is an important factor in the progress of sepsis. Endothelial progenitor cells (EPCs) are the precursor cells of endothelial cells and play a crucial role in the prognosis and treatment of sepsis. EPCs in the peripheral blood of patients with sepsis undergo pyroptosis, but the mechanism remains much of unknown. Serum high-mobility group box-1 (HMGB1) is significantly elevated in patients with sepsis, but whether it is related to EPCs pyroptosis is unknown. We used a cell model of sepsis in vitro to isolate EPCs for better observation. By detecting the pyroptosis-related indicators of EPCs and the level of release and acetylation of HMGB1 in inflammatory macrophages, it was found that HMGB1 released by inflammatory macrophages combined with receptor for advanced glycation end products (RAGE) is a key pathway to induce pyroptosis of EPCs.
引用
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页数:15
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