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小胶质细胞负调控卒中后小鼠脑源性神经干细胞/祖细胞的增殖和神经元分化。

Microglia Negatively Regulate the Proliferation and Neuronal Differentiation of Neural Stem/Progenitor Cells Isolated from Poststroke Mouse Brains.

机构信息

Department of Otorhinolaryngology-Head & Neck Surgery, Hyogo Medical University, 1-1 Mukogawa, Nishinomiya 663-8501, Japan.

Institute for Advanced Medical Sciences, Hyogo Medical University, 1-1 Mukogawacho, Nishinomiya 663-8501, Japan.

出版信息

Cells. 2023 Aug 10;12(16):2040. doi: 10.3390/cells12162040.

DOI:10.3390/cells12162040
PMID:37626850
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10453473/
Abstract

We previously demonstrated that neural stem/progenitor cells (NSPCs) were induced within and around the ischemic areas in a mouse model of ischemic stroke. These injury/ischemia-induced NSPCs (iNSPCs) differentiated to electrophysiologically functional neurons in vitro, indicating the presence of a self-repair system following injury. However, during the healing process after stroke, ischemic areas were gradually occupied by inflammatory cells, mainly microglial cells/macrophages (MGs/MΦs), and neurogenesis rarely occurred within and around the ischemic areas. Therefore, to achieve neural regeneration by utilizing endogenous iNSPCs, regulation of MGs/MΦs after an ischemic stroke might be necessary. To test this hypothesis, we used iNSPCs isolated from the ischemic areas after a stroke in our mouse model to investigate the role of MGs/MΦs in iNSPC regulation. In coculture experiments, we show that the presence of MGs/MΦs significantly reduces not only the proliferation but also the differentiation of iNSPCs toward neuronal cells, thereby preventing neurogenesis. These effects, however, are mitigated by MG/MΦ depletion using clodronate encapsulated in liposomes. Additionally, gene ontology analysis reveals that proliferation and neuronal differentiation are negatively regulated in iNSPCs cocultured with MGs/MΦs. These results indicate that MGs/MΦs negatively impact neurogenesis via iNSPCs, suggesting that the regulation of MGs/MΦs is essential to achieve iNSPC-based neural regeneration following an ischemic stroke.

摘要

我们之前证明，在缺血性中风的小鼠模型中，神经干细胞/祖细胞（NSPCs）在缺血区域内和周围被诱导。这些损伤/缺血诱导的 NSPCs（iNSPCs）在体外分化为具有电生理功能的神经元，表明在损伤后存在自我修复系统。然而，在中风后的愈合过程中，缺血区域逐渐被炎症细胞（主要是小胶质细胞/巨噬细胞（MGs/MΦs））占据，并且很少有神经发生发生在缺血区域内和周围。因此，为了通过利用内源性 iNSPCs 实现神经再生，对缺血性中风后 MGs/MΦs 的调节可能是必要的。为了验证这一假设，我们使用从我们的小鼠模型中风后缺血区域分离的 iNSPCs 来研究 MGs/MΦs 在 iNSPC 调节中的作用。在共培养实验中，我们表明 MGs/MΦs 的存在不仅显著降低了 iNSPCs 向神经元细胞的增殖，而且还降低了其分化，从而阻止了神经发生。然而，用脂质体包裹的 clodronate 耗尽 MG/MΦ 可以减轻这些影响。此外，基因本体分析表明，与 MGs/MΦ 共培养的 iNSPCs 的增殖和神经元分化受到负调控。这些结果表明，MGs/MΦs 通过 iNSPCs 对神经发生产生负面影响，这表明调节 MGs/MΦs 是实现缺血性中风后基于 iNSPC 的神经再生的必要条件。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/ddc785cc0c9b/cells-12-02040-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/446078291df9/cells-12-02040-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/c83b4f93331e/cells-12-02040-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/93a8b0faf3e7/cells-12-02040-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/66802109e15a/cells-12-02040-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/32cb58be22fd/cells-12-02040-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/f669cef2acf2/cells-12-02040-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/ddc785cc0c9b/cells-12-02040-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/446078291df9/cells-12-02040-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/c83b4f93331e/cells-12-02040-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/93a8b0faf3e7/cells-12-02040-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/66802109e15a/cells-12-02040-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/32cb58be22fd/cells-12-02040-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/f669cef2acf2/cells-12-02040-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4852/10453473/ddc785cc0c9b/cells-12-02040-g007.jpg

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