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工程化巨噬细胞膜包裹 S100A9-siRNA 改善心肌缺血再灌注损伤。

Engineered Macrophage Membrane-Coated S100A9-siRNA for Ameliorating Myocardial Ischemia-Reperfusion Injury.

机构信息

Nanjing Drum Tower Hospital, Drum Tower Clinical College, Nanjing University of Chinese Medicine, No. 321 Zhongshan Road, Nanjing, 210008, China.

Department of Cardiology, Affiliated Hospital of Nantong University, Nantong, 226001, China.

出版信息

Adv Sci (Weinh). 2024 Nov;11(41):e2403542. doi: 10.1002/advs.202403542. Epub 2024 Sep 12.

DOI:10.1002/advs.202403542
PMID:39264262
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11538685/
Abstract

Despite the widespread adoption of emergency coronary reperfusion therapy, reperfusion-induced myocardial injury remains a challenging issue in clinical practice. Following myocardial reperfusion, S100A8/A9 molecules are considered pivotal in initiating and regulating tissue inflammatory damage. Effectively reducing the S100A8/A9 level in ischemic myocardial tissue holds significant therapeutic value in salvaging damaged myocardium. In this study, HA (hemagglutinin)- and RAGE (receptor for advanced glycation end products)- comodified macrophage membrane-coated siRNA nanoparticles (MMM/RNA NPs) with siRNA targeting S100A9 (S100A9-siRNA) are successfully prepared. This nanocarrier system is able to target effectively the injured myocardium in an inflammatory environment while evading digestive damage by lysosomes. In vivo, migration of MMM/RNA NPs to myocardial injury lesions is confirmed in a myocardial ischemia-reperfusion injury (MIRI) mouse model. Intravenous injection of MMM/RNA NPs significantly reduced S100A9 levels in serum and myocardial tissues, further decreasing myocardial infarction area and improving cardiac function. Targeted reduction of S100A8/A9 by genetically modified macrophage membrane-coated nanoparticles may represent a new therapeutic intervention for MIRI.

摘要

尽管广泛采用了紧急冠状动脉再灌注治疗，但再灌注引起的心肌损伤仍然是临床实践中的一个挑战。心肌再灌注后，S100A8/A9 分子被认为是启动和调节组织炎症损伤的关键因素。有效降低缺血性心肌组织中的 S100A8/A9 水平对挽救受损心肌具有重要的治疗价值。在这项研究中，成功制备了靶向 S100A9 的 siRNA（S100A9-siRNA）的 HA（血凝素）和 RAGE（晚期糖基化终产物受体）共修饰的巨噬细胞膜包覆的 siRNA 纳米颗粒（MMM/RNA NPs）。该纳米载体系统能够在炎症环境中靶向有效损伤的心肌，同时避免溶酶体的消化损伤。在体内，在心肌缺血再灌注损伤（MIRI）小鼠模型中证实了 MMM/RNA NPs 向心肌损伤病变的迁移。静脉注射 MMM/RNA NPs 可显著降低血清和心肌组织中的 S100A9 水平，进一步减少心肌梗死面积并改善心功能。通过基因修饰的巨噬细胞膜包覆的纳米颗粒靶向减少 S100A8/A9 可能代表 MIRI 的一种新的治疗干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/d32bd9e37b70/ADVS-11-2403542-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/f6c941db1020/ADVS-11-2403542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/d32bd9e37b70/ADVS-11-2403542-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/4a73235f485c/ADVS-11-2403542-g009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/0c9f29cbd4f7/ADVS-11-2403542-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/7167ebb76035/ADVS-11-2403542-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/f6c941db1020/ADVS-11-2403542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ccb/11538685/d32bd9e37b70/ADVS-11-2403542-g008.jpg

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