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KMID : 0892920190280040458
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Experimental Neurobiology
2019 Volume.28 No. 4 p.458 ~ p.473
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Increased CD68/TGFβ Co-expressing Microglia/ Macrophages after Transient Middle Cerebral Artery Occlusion in Rhesus Monkeys
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Yeo Hyeon-Gu
Hong Jung-Joo
Lee Young-Jeon
Yi Kyung-Sik
Jeon Chang-Yeop
Park Jung-Hyung
Won Jin-Young
Seo Jin-Cheol
Ahn Yu-Jin
Kim Keon-Woo
Baek Seung-Ho
Hwang Eun-Ha
Kim Green
Jin Yeung-Bae
Jeong Kang-Jin
Koo Bon-Sang
Kang Phil-Yong
Lim Kyung-Seob
Kim Sun-Uk
Huh Jae-Won
Kim Young-Hyun
Son Yeong-Hoon
Kim Ji-Su
Choi Chi-Hoon
Cha Sang-Hoon
Lee Sang-Rae
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Abstract
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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 colocalized 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.
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KEYWORD
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Inflammation, Microglia, Stroke, Macaca mulatta, Transforming growth factor beta
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