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人脐带间充质干细胞外泌体通过促进NLRP3泛素化来预防缺氧缺血性脑损伤。

hUC-MSC extracellular vesicles protect against hypoxic-ischemic brain injury by promoting NLRP3 ubiquitination.

作者信息

Xiao Shanshan, Lv Ying, Hou Xuejing, Qu Shuqiang

机构信息

Department of Pediatrics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Department of Pediatrics, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.

出版信息

Biomol Biomed. 2025 May 8;25(7):1553-1570. doi: 10.17305/bb.2024.10706.


DOI:10.17305/bb.2024.10706
PMID:39739400
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12097387/
Abstract

Hypoxic-ischemic brain injury (HIBD) is a major cause of neonatal mortality and long-term neurological deficits, with limited treatment options. Extracellular vesicles (EVs) from human umbilical cord mesenchymal stem cells (hUC-MSC-EVs) have shown promise in neuroprotection, but the mechanisms remain unclear. This study explores how hUC-MSC-EVs protect neonatal rats from HIBD. hUC-MSC-EVs were isolated, characterized, and administered to neonatal rats subjected to HIBD. Behavioral reflexes and brain infarction were assessed, along with cellular and molecular analyses of hippocampal tissue. An in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model was used to simulate ischemic conditions in rat primary microglia. Results demonstrated that hUC-MSC-EVs significantly improved neurological outcomes, reduced brain infarction, and decreased microglial activation and pyroptosis. These effects were linked to the inhibition of NLRP3 inflammasome activation and enhanced ubiquitination via the protein kinase A (PKA) pathway. Blocking PKA partially reversed these protective effects. Here we highlight that hUC-MSC-EVs provide neuroprotection by regulating the NLRP3 inflammasome, offering a potential therapeutic strategy for HIBD. These findings expand the understanding of EV-mediated neuroprotection and suggest broader applications for ischemia-related conditions, with potential for clinical translation.

摘要

缺氧缺血性脑损伤(HIBD)是新生儿死亡和长期神经功能缺损的主要原因,治疗选择有限。人脐带间充质干细胞来源的细胞外囊泡(hUC-MSC-EVs)已显示出神经保护作用,但机制尚不清楚。本研究探讨hUC-MSC-EVs如何保护新生大鼠免受HIBD损伤。分离、鉴定hUC-MSC-EVs,并将其给予遭受HIBD的新生大鼠。评估行为反射和脑梗死情况,同时对海马组织进行细胞和分子分析。使用体外氧糖剥夺/复氧(OGD/R)模型模拟大鼠原代小胶质细胞的缺血状态。结果表明,hUC-MSC-EVs显著改善神经功能结局,减少脑梗死,降低小胶质细胞活化和焦亡。这些作用与通过蛋白激酶A(PKA)途径抑制NLRP3炎性小体活化和增强泛素化有关。阻断PKA可部分逆转这些保护作用。在此我们强调,hUC-MSC-EVs通过调节NLRP3炎性小体提供神经保护,为HIBD提供了一种潜在的治疗策略。这些发现扩展了对EV介导的神经保护的理解,并提示其在缺血相关疾病中的更广泛应用,具有临床转化潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/62bbaf57b514/bb-2024-10706f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/4f7add569643/bb-2024-10706f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/1095b63edb95/bb-2024-10706f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/8b9e48c56e0d/bb-2024-10706f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/67cdd777b709/bb-2024-10706f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/1f3dbdff3914/bb-2024-10706f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/f0fac23d111e/bb-2024-10706f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/183a134efbe3/bb-2024-10706f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/62bbaf57b514/bb-2024-10706f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/4f7add569643/bb-2024-10706f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/1095b63edb95/bb-2024-10706f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/8b9e48c56e0d/bb-2024-10706f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/67cdd777b709/bb-2024-10706f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/1f3dbdff3914/bb-2024-10706f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/f0fac23d111e/bb-2024-10706f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/183a134efbe3/bb-2024-10706f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/555d/12097387/62bbaf57b514/bb-2024-10706f8.jpg

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本文引用的文献

[1]
Overexpression of USP35 enhances the protective effect of hUC-MSCs and their extracellular vesicles in oxygen-glucose deprivation/reperfusion-induced SH-SY5Y cells via stabilizing FUNDC1.

Commun Biol. 2024-10-15

[2]
Identification and analysis of oxidative stress-related genes in hypoxic-ischemic brain damage using bioinformatics and experimental verification.

Immun Inflamm Dis. 2024-8

[3]
Extracellular vesicles as mediators of stress response in embryo-maternal communication.

Front Cell Dev Biol. 2024-8-5

[4]
Cell Type-Specific Extracellular Vesicles and Their Impact on Health and Disease.

Int J Mol Sci. 2024-2-27

[5]
Hidradenitis Suppurativa: An Understanding of Genetic Factors and Treatment.

Biomedicines. 2024-2-1

[6]
Inactivation of the NLRP3 inflammasome mediates exosome-based prevention of atrial fibrillation.

Theranostics. 2024

[7]
Comparative Proteomics Inspired Self-Stimulated Release Hydrogel Reinforces the Therapeutic Effects of MSC-EVs on Alzheimer's Disease.

Adv Mater. 2024-4

[8]
Neuroprotective Effects of Human-Induced Pluripotent Stem Cell-Derived Mesenchymal Stem Cell Extracellular Vesicles in Ischemic Stroke Models.

Biomedicines. 2023-9-17

[9]
MiR-126 and miR-146a as Melatonin-Responsive Biomarkers for Neonatal Brain Ischemia.

J Mol Neurosci. 2023-10

[10]
Inhibiting NLRP3 inflammasome signaling pathway promotes neurological recovery following hypoxic-ischemic brain damage by increasing p97-mediated surface GluA1-containing AMPA receptors.

J Transl Med. 2023-8-24

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