Triggering Receptor Expressed on Myeloid Cells-2 Correlates to Hypothermic Neuroprotection in Ischemic Stroke

Kawabori, Masahito; Hokari, Masaaki; Zheng, Zhen; Kim, Jong Youl; Calosing, Cyrus; Hsieh, Christine L.; Nakamura, Mary C.; Yenari, Midori A.

Triggering Receptor Expressed on Myeloid Cells-2 Correlates to Hypothermic Neuroprotection in Ischemic Stroke

Kawabori, Masahito; Hokari, Masaaki; Zheng, Zhen et al.

Therapeutic Hypothermia and Temperature Management, 2013, 3(4), 189-198

Permalink : https://hdl.handle.net/2115/70809

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アクセス権	open access
URI	https://hdl.handle.net/2115/70809
タイトル	Triggering Receptor Expressed on Myeloid Cells-2 Correlates to Hypothermic Neuroprotection in Ischemic Stroke
その他のタイトル	TREM-2 in hypothermia
著者	Kawabori, Masahito ; Hokari, Masaaki ; Zheng, Zhen ; Kim, Jong Youl ; Calosing, Cyrus ; Hsieh, Christine L. ; Nakamura, Mary C. ; Yenari, Midori A.
e-Rad_Researcher 50399870 著者名 Kawabori, Masahito
e-Rad_Researcher 30622807 著者名 Hokari, Masaaki
著者名 Zheng, Zhen
著者名 Kim, Jong Youl
著者名 Calosing, Cyrus
著者名 Hsieh, Christine L.
著者名 Nakamura, Mary C.
著者名 Yenari, Midori A.
言語	英語
キーワード	brain ischemia
	inflammation
	neuroprotection
	stroke
	TREM2
発行日	2013-12
出版者	Mary Ann Liebert
収録物名	Therapeutic Hypothermia and Temperature Management
巻(号)	3(4)
ページ	189-198
抄録	Hypothermia is neuroprotective against many acute neurological insults including ischemic stroke. We and others have previously shown that protection by hypothermia is partially associated with the suppression of the inflammatory. Phagocytes are thought to play an important role in the clearance of necrotic debris, paving the way for endogenous repair mechanisms to commence, but the effect of cooling and phagocytosis has not been extensively studied. Triggering receptor expressed on myeloid cells-2 (TREM2) is a newly identified surface receptor shown to be involved in phagocytosis. In this study, we examined the effect of therapeutic hypothermia on TREM2 expression. Mice underwent permanent middle cerebral artery occlusion (MCAO) and were treated with one of 2 cooling paradigms: one where cooling (30 C) began at the onset of MCAO (early hypothermia) and another where cooling began 1h later (delayed hypothermia). In both groups, cooling was maintained for 2h. A 3rd group was maintained at normothermia as a control (37C). Mice from the normothermia and delayed hypothermia groups had similar ischemic lesions sizes and neurological performance, but early hypothermia group showed marked protection as evidenced by smaller lesion size and less neurological deficits up to 30 days after the insult. Microglia and macrophages increased after MCAO as early as 3 days, peaked at 7 days, and decreased by 14 days. Both hypothermia paradigms were associated with decreased numbers of microglia and macrophages at 3 and 7 days, with greater decreases in the early paradigm. However, the proportion of the TREM2 positive microglia/macrophages was actually increased among the early hypothermia group at day 7. Early hypothermia showed long term neurological benefit, but neuroprotection did not correlate to immune suppression. However, hypothermic neuroprotection was associated with relative increased in TREM2 expression, and suggests that TREM2 may serve a beneficial role in brain ischemia.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	Final publication is available from Mary Ann Liebert, Inc., publishers http://dx.doi.org/10.1089/ther.2013.0020
PISSN	2153-7658
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1089/ther.2013.0020