Exosome-mediated pyroptosis of miR-93-TXNIP-NLRP3 leads to functional difference between M1 and M2 macrophages in sepsis-induced acute kidney injury.
Exosome-mediated pyroptosis of miR-93-TXNIP-NLRP3 leads to functional difference between M1 and M2 macrophages in sepsis-induced acute kidney injury.
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外泌体介导的miR-93-TXNIP-NLRP 3的焦亡导致M1和M2巨噬细胞在脓毒症诱导的急性肾损伤中的功能差异
DOI：
10.1111/jcmm.16449
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发表时间：
2021-05
影响因子：
5.3
通讯作者：
Jin R
中科院分区：
文献类型：
--
作者：
Juan CX;Mao Y;Cao Q;Chen Y;Zhou LB;Li S;Chen H;Chen JH;Zhou GP;Jin R
Sepsis is a systemic inflammatory response syndrome caused by infection, resulting in organ dysfunction. Sepsis‐induced acute kidney injury (AKI) is one of the most common potential complications. Increasing reports have shown that M1 and M2 macrophages both take part in the progress of AKI by influencing the level of inflammatory factors and the cell death, including pyroptosis. However, whether M1 and M2 macrophages regulate AKI by secreting exosome remains unknown. In the present study, we isolated the exosomes from M1 and M2 macrophages and used Western blot and enzyme‐linked immunosorbent assay (ELISA) to investigate the effect of M1 and M2 exosomes on cell pyroptosis. miRNA sequencing was used to identify the different miRNA in M1 and M2 exosomes. Luciferase reporter assay was used to verify the target gene of miRNA. We confirmed that exosomes excreted by macrophages regulated cell pyroptosis in vitro by using Western blot and ELISA. miRNA sequencing revealed the differentially expressed level of miRNAs in M1 and M2 exosomes, among which miR‐93‐5p was involved in the regulation of pyroptosis. By using bioinformatics predictions and luciferase reporter assay, we found that thioredoxin–interacting protein (TXNIP) was a direct target of miR‐93‐5p. Further in vitro and in vivo experiments indicated that exosomal miR‐93‐5p regulated the TXNIP directly to influence the pyroptosis in renal epithelial cells, which explained the functional difference between different phenotypes of macrophages. This study might provide new targets for the treatment of sepsis‐induced AKI.
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影响因子：
16.6
作者：
Teng Y;Ren Y;Hu X;Mu J;Samykutty A;Zhuang X;Deng Z;Kumar A;Zhang L;Merchant ML;Yan J;Miller DM;Zhang HG
通讯作者：
Zhang HG
DOI：
10.1038/s41581-018-0103-6
发表时间：
2019-04
期刊：
Nature reviews. Nephrology
影响因子：
--
作者：
Guo C;Dong G;Liang X;Dong Z
通讯作者：
Dong Z
影响因子：
3.7
作者：
Chung SD;Lai TY;Chien CT;Yu HJ
通讯作者：
Yu HJ
影响因子：
5.7
作者：
Fehlmann T;Reinheimer S;Geng C;Su X;Drmanac S;Alexeev A;Zhang C;Backes C;Ludwig N;Hart M;An D;Zhu Z;Xu C;Chen A;Ni M;Liu J;Li Y;Poulter M;Li Y;Stähler C;Drmanac R;Xu X;Meese E;Keller A
通讯作者：
Keller A
影响因子：
16.6
作者：
Kimura K;Hohjoh H;Fukuoka M;Sato W;Oki S;Tomi C;Yamaguchi H;Kondo T;Takahashi R;Yamamura T
通讯作者：
Yamamura T