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恒河猴短暂性大脑中动脉闭塞后共表达CD68/TGFβ的小胶质细胞/巨噬细胞增加。

Increased CD68/TGFβ Co-expressing Microglia/ Macrophages after Transient Middle Cerebral Artery Occlusion in Rhesus Monkeys.

作者信息

Yeo Hyeon-Gu, Hong Jung Joo, Lee Youngjeon, Yi Kyung Sik, Jeon Chang-Yeop, Park Junghyung, Won Jinyoung, Seo Jincheol, Ahn Yu-Jin, Kim Keonwoo, Baek Seung Ho, Hwang Eun-Ha, Kim Green, Jin Yeung Bae, Jeong Kang-Jin, Koo Bon-Sang, Kang Philyong, Lim Kyung Seob, Kim Sun-Uk, Huh Jae-Won, Kim Young-Hyun, Son Yeonghoon, Kim Ji-Su, Choi Chi-Hoon, Cha Sang-Hoon, Lee Sang-Rae

机构信息

National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju 28116, Korea.

Department of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon 34113, Korea.

出版信息

Exp Neurobiol. 2019 Aug 31;28(4):458-473. doi: 10.5607/en.2019.28.4.458.

DOI:10.5607/en.2019.28.4.458
PMID:31495075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6751863/
Abstract

The function of microglia/macrophages after ischemic stroke is poorly understood. This study examines the role of microglia/macrophages in the focal infarct area after transient middle cerebral artery occlusion (MCAO) in rhesus monkeys. We measured infarct volume and neurological function by magnetic resonance imaging (MRI) and non-human primate stroke scale (NHPSS), respectively, to assess temporal changes following MCAO. Activated phagocytic microglia/macrophages were examined by immunohistochemistry in post-mortem brains (n=6 MCAO, n=2 controls) at 3 and 24 hours (acute stage), 2 and 4 weeks (subacute stage), and 4, and 20 months (chronic stage) following MCAO. We found that the infarct volume progressively decreased between 1 and 4 weeks following MCAO, in parallel with the neurological recovery. Greater presence of cluster of differentiation 68 (CD68)-expressing microglia/macrophages was detected in the infarct lesion in the subacute and chronic stage, compared to the acute stage. Surprisingly, 98~99% of transforming growth factor beta (TGFβ) was found co-localized with CD68-expressing cells. CD68-expressing microglia/macrophages, rather than CD206 cells, may exert anti-inflammatory effects by secreting TGFβ after the subacute stage of ischemic stroke. CD68 microglia/macrophages can therefore be used as a potential therapeutic target.

摘要

缺血性中风后小胶质细胞/巨噬细胞的功能尚不清楚。本研究探讨了小胶质细胞/巨噬细胞在恒河猴短暂性大脑中动脉闭塞（MCAO）后局灶性梗死区域中的作用。我们分别通过磁共振成像（MRI）和非人灵长类动物中风量表（NHPSS）测量梗死体积和神经功能，以评估MCAO后的时间变化。在MCAO后3小时和24小时（急性期）、2周和4周（亚急性期）以及4个月和20个月（慢性期），通过免疫组织化学在死后大脑中检查活化的吞噬性小胶质细胞/巨噬细胞（n = 6 MCAO，n = 2对照）。我们发现，MCAO后1至4周梗死体积逐渐减小，与神经功能恢复同步。与急性期相比，在亚急性期和慢性期的梗死灶中检测到更多表达分化簇68（CD68）的小胶质细胞/巨噬细胞。令人惊讶的是，发现98%至99%的转化生长因子β（TGFβ）与表达CD68的细胞共定位。在缺血性中风亚急性期后，表达CD68的小胶质细胞/巨噬细胞而非CD206细胞可能通过分泌TGFβ发挥抗炎作用。因此，CD68小胶质细胞/巨噬细胞可作为潜在的治疗靶点。

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