Increased CD68/TGFβ Co-expressing Microglia/Macrophages after Transient Middle Cerebral Artery Occlusion in Rhesus Monkeys
- Author:
Hyeon Gu YEO
1
;
Jung Joo HONG
;
Youngjeon LEE
;
Kyung Sik YI
;
Chang Yeop JEON
;
Junghyung PARK
;
Jinyoung WON
;
Jincheol SEO
;
Yu Jin AHN
;
Keonwoo KIM
;
Seung Ho BAEK
;
Eun Ha HWANG
;
Green KIM
;
Yeung Bae JIN
;
Kang Jin JEONG
;
Bon Sang KOO
;
Philyong KANG
;
Kyung Seob LIM
;
Sun Uk KIM
;
Jae Won HUH
;
Young Hyun KIM
;
Yeonghoon SON
;
Ji Su KIM
;
Chi Hoon CHOI
;
Sang Hoon CHA
;
Sang Rae LEE
Author Information
- Publication Type:Original Article
- Keywords: Inflammation; Microglia; Stroke; Macaca mulatta; Transforming growth factor beta
- MeSH: Brain; Haplorhini; Immunohistochemistry; Infarction, Middle Cerebral Artery; Inflammation; Macaca mulatta; Magnetic Resonance Imaging; Microglia; Middle Cerebral Artery; Primates; Stroke; Transforming Growth Factor beta
- From:Experimental Neurobiology 2019;28(4):458-473
- CountryRepublic of Korea
- Language:English
- 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 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.
