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

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Title: Triggering Receptor Expressed on Myeloid Cells-2 Correlates to Hypothermic Neuroprotection in Ischemic Stroke
Other Titles: TREM-2 in hypothermia
Authors: Kawabori, Masahito Browse this author →KAKEN DB
Hokari, Masaaki Browse this author →KAKEN DB
Zheng, Zhen Browse this author
Kim, Jong Youl Browse this author
Calosing, Cyrus Browse this author
Hsieh, Christine L. Browse this author
Nakamura, Mary C. Browse this author
Yenari, Midori A. Browse this author
Keywords: brain ischemia
Issue Date: Dec-2013
Publisher: Mary Ann Liebert
Journal Title: Therapeutic Hypothermia and Temperature Management
Volume: 3
Issue: 4
Start Page: 189
End Page: 198
Publisher DOI: 10.1089/ther.2013.0020
Abstract: 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.
Rights: Final publication is available from Mary Ann Liebert, Inc., publishers
Type: article (author version)
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 川堀 真人

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