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Platelet Exosome-Derived miR-223-3p Regulates Pyroptosis in the Cell Model of Sepsis-Induced Acute Renal Injury by Targeting Mediates NLRP3

败血症 医学 急性肾损伤 血小板 外体 脂多糖 上睑下垂 免疫学 微泡 血小板活化 炎症 内科学 炎症体 化学 小RNA 生物化学 基因
作者
Peng Wan,Xiang Tan,Mengting Sheng,Yan Xiang,Peng Wang,Min Yu
出处
期刊:Critical Reviews in Immunology 卷期号:44 (3): 53-65
标识
DOI:10.1615/critrevimmunol.2023051651
摘要

<b>Background:</b> The present study investigated the roles and mechanisms of platelet-derived exosomes in sepsis-induced acute renal injury. <b>Methods:</b> The blood samples of septic patients and healthy controls were collected for clinical examination. The plasma levels of miR-223-3p and NLRP3 mRNA were analyzed by qRT-PCR and the serum IL-1&beta; and creatinine levels were quantified by enzyme-linked immunosorbent assay (ELISA). C57BL/6 mice injected with LPS (lipopolysaccharide) were employed as the animal model for sepsis-induced acute renal injury. Human coronary artery endothelial cells (HCAECs) were treated with TNF-&alpha; as a cellular model for sepsis-induced endothelial damages. <b>Results: </b>The number of PMP (platelet-derived microparticles) in patients with sepsis was increased. The level of miR-223-3p in the platelet exosomes isolated from the serum sample in patients with sepsis was significantly lower than that of the healthy controls. The level of miR-223-3p was also decreased in the platelet exosomes of mouse model with sepsis-induced acute renal injury. Downregulating miR-223-3p promoted sepsis-induced acute renal injury in mice model, while the administration of miR-223-3p reduced the inflammation in endothelial cells of sepsis-induced acute renal injury. NLRP3 (NLR Family Pyrin Domain Containing 3) was identified as one target of miR-223-3p in the platelet exosomes of sepsis-induced acute kidney injury. miR-223-3p attenuated NLRP3-induced pyroptosis in endothelial cell model of sepsis-induced acute kidney injury. <b>Conclusion:</b> Our data suggest that platelet exosome-derived miR-223-3p negatively regulates NLRP3-dependent inflammasome to suppress pyroptosis in endothelial cells. Decreased miR-223-3p expression promotes the inflammation in sepsis-induced acute renal injury. Targeting miR-223-3p may be developed into a therapeutic approach for sepsis-induced acute renal injury.

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