Exosomes derived from bone marrow mesenchymal stem cells regulate pyroptosis via the miR-143-3p/myeloid differentiation factor 88 axis to ameliorate intestinal ischemia-reperfusion injury.
Exosomes derived from bone marrow mesenchymal stem cells regulate pyroptosis via the miR-143-3p/myeloid differentiation factor 88 axis to ameliorate intestinal ischemia-reperfusion injury.
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源自骨髓间充质干细胞的外泌体通过 miR-143-3p/骨髓分化因子 88 轴调节细胞焦亡，以改善肠道缺血再灌注损伤。
DOI：
10.1080/21655979.2023.2253414
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发表时间：
2023-12
期刊：
影响因子：
4.9
通讯作者：
中科院分区：
文献类型：
--
作者：
肠缺血-再灌注（I/R）损伤是缺血后由于血供恢复而使组织损伤加重的情况。骨髓间充质干细胞来源的exosome（BMSC-exo）对I/R损伤具有保护作用。本研究旨在探讨BMSC-exos改善肠I/R损伤的可能机制。我们通过超离心分离小鼠BMSC-exos，发现它们在细胞模型中有效地增加细胞活力，减轻小鼠模型中的肠屏障损伤，并下调炎性细胞因子和pyroptosis相关蛋白的表达，表明BMSC-exos可能通过调节pyroptosis减轻体外和体内肠I/R损伤。我们通过微阵列测序鉴定了miR-143- 3 p作为差异表达的miRNA。生物信息学分析预测了miR-143- 3 p与髓样分化因子88（MyD 88）之间的结合位点;双荧光素酶报告基因分析证实了miR-143- 3 p可以直接调控MyD 88的表达。我们的研究结果表明，miR-143- 3 p通过调节NOD样受体热蛋白结构域相关蛋白3（NLRP 3）通过toll样受体（TLR）-4/MyD88/核因子κ-B（NF-κ B）途径调节细胞凋亡。本研究描述了使用BMSC-exos治疗肠I/R损伤的潜在策略，BMSC-exos通过miR-143- 3 p介导的TLR 4/MyD 88/NF-кB途径调节细胞凋亡。BMSC-exos改善肠缺血/再灌注（I/R）损伤miR-143- 3 p水平在I/R损伤中降低并且随着BMSC-exo治疗而升高miR-143- 3 p直接靶向并下调MyD 88的表达BMSC-exos通过miR-143- 3 p-MyD 88轴调节肠I/R损伤中的焦亡
Intestinal ischemia-reperfusion (I/R) injury is a condition in which tissue injury is aggravated after ischemia due to recovery of blood supply. Bone marrow mesenchymal stem cell-derived exosome (BMSC-exo) showed a protective effect on I/R injury. This study aimed to investigate the possible mechanisms by which BMSC-exos ameliorate intestinal I/R injury. We isolated mouse BMSC-exos by super-centrifugation and found that they effectively increased cell viability in a cell model, alleviated intestinal barrier injury in a mouse model, and downregulated the expression of inflammatory cytokines and pyroptosis-related proteins, suggesting that BMSC-exos may alleviate intestinal I/R injury in vitro and in vivo by regulating pyroptosis. We identified miR-143-3p as a differentially expressed miRNA by microarray sequencing. Bioinformatic analysis predicted a binding site between miR-143-3p and myeloid differentiation factor 88 (MyD88); a dual-luciferase reporter assay confirmed that miR-143-3p could directly regulate the expression of MyD88. Our findings suggest that miR-143-3p regulates pyroptosis by regulating NOD-like receptor thermal protein domain associated protein 3 (NLRP3) through the toll-like receptor (TLR)-4/MyD88/nuclear factor kappa-B (NF-кB) pathway. This study describes a potential strategy for the treatment of intestinal I/R injury using BMSC-exos that act by regulating pyroptosis through the miR-143-3p mediated TLR4/MyD88/NF-кB pathway. BMSC-exos ameliorate intestinal ischemia/reperfusion (I/R) injury miR-143-3p levels were reduced in I/R injury and increased with BMSC-exo treatment miR-143-3p directly targeted and downregulated the expression of MyD88 BMSC-exos regulate pyroptosis in intestinal I/R injury via the miR-143-3p-MyD88 axis
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