Engineered neutrophil apoptotic bodies ameliorate myocardial infarction by promoting macrophage efferocytosis and inflammation resolution.
Engineered neutrophil apoptotic bodies ameliorate myocardial infarction by promoting macrophage efferocytosis and inflammation resolution.
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工程化中性粒细胞凋亡小体通过促进巨噬细胞胞吞作用和炎症消退来改善心肌梗死。
DOI：
10.1016/j.bioactmat.2021.08.008
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发表时间：
2022-03
影响因子：
18.9
通讯作者：
Jin Y
中科院分区：
文献类型：
--
作者：
Bao L;Dou G;Tian R;Lv Y;Ding F;Liu S;Zhao R;Zhao L;Zhou J;Weng L;Dong Y;Li B;Liu S;Chen X;Jin Y
炎症反应在心肌梗死(MI)修复中起着至关重要的作用。中性粒细胞凋亡和随后的巨噬细胞摄取可以导致炎症消退和启动再生，而模拟和加强这一自然过程的治疗策略尚未建立。在这里，我们构建了工程化的中性粒细胞凋亡小体(ENAB)来模拟自然的中性粒细胞凋亡，它调节炎症反应和增强心肌梗死修复。将具有良好致炎和免疫调节特性的天然中性粒细胞凋亡小体膜与负载5-氨基乙酰丙酸己酯(HAL)的介孔二氧化硅纳米颗粒相结合，制备了eNAbs。主动靶向巨噬细胞的eNAbs和包裹的HAL同时启动了血红素的生物合成途径，在细胞内释放后产生抗炎胆红素，从而进一步增强了抗炎作用。在体内研究中，eNAbs有效地调节了梗死区的炎症反应，以改善心功能。这项研究证明了一种有效的仿生构建策略来调节巨噬细胞对心肌梗死修复的功能。构建模拟自然中性粒细胞凋亡的工程化中性粒细胞凋亡小体。工程化的中性粒细胞凋亡小体，具有良好的趋炎性和巨噬细胞特异性靶向能力。工程化的中性粒细胞凋亡小体增强巨噬细胞的吞噬作用和重新编程以消解炎症。工程化中性粒细胞凋亡体可改善心肌梗死并促进心肌梗死后的心肌组织再生。
Inflammatory response plays a critical role in myocardial infarction (MI) repair. The neutrophil apoptosis and subsequent macrophage ingestion can result in inflammation resolution and initiate regeneration, while the therapeutic strategy that simulates and enhances this natural process has not been established. Here, we constructed engineered neutrophil apoptotic bodies (eNABs) to simulate natural neutrophil apoptosis, which regulated inflammation response and enhanced MI repair. The eNABs were fabricated by combining natural neutrophil apoptotic body membrane which has excellent inflammation-tropism and immunoregulatory properties, and mesoporous silica nanoparticles loaded with hexyl 5-aminolevulinate hydrochloride (HAL). The eNABs actively targeted to macrophages and the encapsulated HAL simultaneously initiated the biosynthesis pathway of heme to produce anti-inflammatory bilirubin after intracellular release, thereby further enhancing the anti-inflammation effects. In in vivo studies, the eNABs efficiently modulated inflammation responses in the infarcted region to ameliorate cardiac function. This study demonstrates an effective biomimetic construction strategy to regulate macrophage functions for MI repair. Construction of engineered neutrophil apoptotic bodies to simulate natural neutrophil apoptosis. Engineered neutrophil apoptotic bodies with excellent inflammation-tropism and macrophage-specific targeting capacity. Engineered neutrophil apoptotic bodies enhance macrophage efferocytosis and reprogramming for inflammation resolution. Engineered neutrophil apoptotic bodies ameliorate myocardial infarction and promote cardiac tissue regeneration after MI.
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凋亡和心脏内注射凋亡白细胞悬浮液可通过在心肌梗塞后增加心脏疤痕组织中的弹性蛋白表达来防止心室重塑。
影响因子：
9.5
作者：
Lichtenauer M;Mildner M;Baumgartner A;Hasun M;Werba G;Beer L;Altmann P;Roth G;Gyöngyösi M;Podesser BK;Ankersmit HJ
通讯作者：
Ankersmit HJ
影响因子：
37.8
作者：
BOYLE, MP;WEISMAN, HF
通讯作者：
WEISMAN, HF
影响因子：
20.3
作者：
Dalli, Jesmond;Norling, Lucy V.;Perretti, Mauro
通讯作者：
Perretti, Mauro
影响因子：
7.3
作者：
Caruso S;Poon IKH
通讯作者：
Poon IKH
影响因子：
8.7
作者：
Greenlee-Wacker MC
通讯作者：
Greenlee-Wacker MC