miR-142-5p Encapsulated by Serum-Derived Extracellular Vesicles Protects against Acute Lung Injury in Septic Rats following Remote Ischemic Preconditioning via the PTEN/PI3K/Akt Axis

IF 4.7 3区 医学 Q2 IMMUNOLOGY Journal of Innate Immunity Pub Date : 2022-05-19 DOI:10.1159/000522231
Wenliang Zhu, Xiaopei Huang, Shi-Yuan Qiu, Lingxiao Feng, Yue Wu, Huanzhang Shao
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引用次数: 1

Abstract

This study intends to investigate the effects of miR-142-5p encapsulated by serum-derived extracellular vesicles (EVs) on septic acute lung injury (ALI) following remote ischemic preconditioning (RIPC) through a PTEN-involved mechanism. ALI was induced in rats by lipopolysaccharide (LPS) injection, 24 h before which RIPC was performed via the left lower limb. Next, the binding affinity between miR-142-5p and PTEN was identified. EVs were isolated from serum and injected into rats. The morphology of lung tissues, pulmonary edema, and inflammatory cell infiltration into lung tissues were then assessed, and TNF-α and IL-6 levels in serum and lung tissues were measured. The results indicated that RIPC could attenuate ALI in sepsis. miR-142-5p expression was increased in serum, lung tissues, and serum-derived EVs of ALI rats following RIPC. miR-142-5p could target PTEN to activate the PI3K/Akt signaling pathway. miR-142-5p shuttled by serum-derived EVs reduced pulmonary edema, neutrophil infiltration, and TNF-α and IL-6 levels, thus alleviating ALI in LPS-induced septic rats upon RIPC. Collectively, serum-derived EVs-loaded miR-142-5p downregulated PTEN and activated PI3K/Akt to inhibit ALI in sepsis following RIPC, thus highlighting potential therapeutic molecular targets against ALI in sepsis.
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经血清源性细胞外囊泡包封的miR-142-5p通过PTEN/PI3K/Akt轴保护脓毒症大鼠远程缺血预处理后的急性肺损伤
本研究旨在通过PTEN相关机制研究血清来源的细胞外小泡(EVs)包裹的miR-142-5p对远程缺血预处理(RIPC)后脓毒症急性肺损伤(ALI)的影响。脂多糖(LPS)注射诱导大鼠ALI,24小时前经左下肢RIPC。接下来,鉴定了miR-142-5p与PTEN之间的结合亲和力。从血清中分离EVs并将其注射到大鼠体内。然后评估肺组织的形态、肺水肿和炎症细胞浸润到肺组织中,并测量血清和肺组织中TNF-α和IL-6的水平。结果表明,RIPC可减轻脓毒症患者的ALI。RIPC后ALI大鼠血清、肺组织和血清衍生EVs中miR-142-5p的表达增加。miR-142-5p可以靶向PTEN激活PI3K/Akt信号通路。血清来源EVs穿梭的miR-142-5p降低了肺水肿、中性粒细胞浸润以及TNF-α和IL-6水平,从而减轻了RIPC后LPS诱导的脓毒症大鼠的ALI。总之,血清来源的EVs负载miR-142-5p下调PTEN并激活PI3K/Akt以抑制RIPC后败血症中的ALI,从而突出了针对败血症中ALI的潜在治疗分子靶点。
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来源期刊
Journal of Innate Immunity
Journal of Innate Immunity 医学-免疫学
CiteScore
10.50
自引率
1.90%
发文量
35
审稿时长
7.5 months
期刊介绍: The ''Journal of Innate Immunity'' is a bimonthly journal covering all aspects within the area of innate immunity, including evolution of the immune system, molecular biology of cells involved in innate immunity, pattern recognition and signals of ‘danger’, microbial corruption, host response and inflammation, mucosal immunity, complement and coagulation, sepsis and septic shock, molecular genomics, and development of immunotherapies. The journal publishes original research articles, short communications, reviews, commentaries and letters to the editors. In addition to regular papers, some issues feature a special section with a thematic focus.
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