Annexin-A5 monomer as a membrane repair agent for the treatment of renal ischemia-reperfusion injury

被引:1
|
作者
Dong, Yushan [1 ,2 ]
Jia, Zhuoxuan [1 ,2 ]
Kang, Bijun [1 ,2 ]
Zhang, Wenjie [1 ,2 ]
机构
[1] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Plast & Reconstruct Surg, Sch Med, Shanghai 200011, Peoples R China
[2] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Shanghai Key Lab Tissue Engn, Sch Med, Shanghai 200011, Peoples R China
关键词
Ischemia-reperfusion injury; Kidney injury; Annexin A5; Membrane repair; Apoptosis; PHOSPHATIDYLSERINE; MECHANISM; INFLAMMATION; SURFACE; CELLS;
D O I
10.1007/s11033-024-09606-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
BackgroundRenal ischemia-reperfusion injury (IRI) is one of the causes of acute kidney injury. Annexin A5 (AnxA5), a calcium-dependent cell membrane-binding protein, shows protective effects in various organ IRI models. This study explored the therapeutic effect of exogenous AnxA5 monomer protein on renal IRI and its potential mechanism of action.Methods and resultsDifferent doses of AnxA5 were injected intravenously to treat bilateral renal IRI in SD rats. This model confirmed the protective effects of AnxA5 on kidney structure and function. In vitro, HK-2 cells were subjected to hypoxia for 12 h, followed by restoration of normal oxygen supply to simulate IRI. In vitro experiments demonstrated the mechanism of action of AnxA5 by measuring cellular activity and permeability. A comparison of the mutant AnxA5 protein M23 and the application of a calcium-free culture medium further validated the protective effect of AnxA5 by forming a network structure.ConclusionsExogenous AnxA5 monomers prevented renal IRI by binding to the damaged renal tubular epithelial cell membrane, forming a two-dimensional network structure to maintain cell membrane integrity, and ultimately prevent cell death.
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页数:14
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