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j.bbrc.2019.05.055.pdf | 882.06 kB | Adobe PDF | 見る/開く |
タイトル: | Depletion of microglia ameliorates white matter injury and cognitive impairment in a mouse chronic cerebral hypoperfusion model |
著者: | Kakae, Masashi Tobori, Shota Morishima, Misa Nagayasu, Kazuki https://orcid.org/0000-0002-7438-732X (unconfirmed) Shirakawa, Hisashi https://orcid.org/0000-0002-4129-0978 (unconfirmed) Kaneko, Shuji https://orcid.org/0000-0001-5152-5809 (unconfirmed) |
著者名の別形: | 抱, 将史 白川, 久志 金子, 周司 |
キーワード: | Chronic cerebral hypoperfusion Cognitive impairment White matter injury Microglia Cytokines Colony-stimulating factor 1 |
発行日: | 5-Jul-2019 |
出版者: | Elsevier BV |
誌名: | Biochemical and Biophysical Research Communications |
巻: | 514 |
号: | 4 |
開始ページ: | 1040 |
終了ページ: | 1044 |
抄録: | Microglia are immune cells in the central nervous system (CNS) and essential for homeostasis that are important for both neuroprotection and neurotoxicity, and are activated in a variety of CNS diseases. Microglia aggravate cognitive impairment induced by chronic cerebral hypoperfusion, but their precise roles under these conditions remain unknown. Here, we used PLX3397, a colony-stimulating factor 1 receptor inhibitor, to deplete microglia in mice with chronic cerebral hypoperfusion induced by bilateral common carotid artery stenosis (BCAS). Cognitive impairment induced 28 days after BCAS was significantly improved in mice fed a diet containing PLX3397. In PLX3397-fed mice, microglia were depleted and white matter injury induced by BCAS was suppressed. In addition, the expression of proinflammatory cytokines, interleukin 6 and tumor necrosis factor alpha, was suppressed in PLX3397-fed mice. Taken together, these findings suggest that microglia play destructive roles in the development of cognitive impairment and white matter injury induced by chronic cerebral hypoperfusion. Thus, microglia represent a potential therapeutic target for chronic cerebral hypoperfusion-related diseases. |
著作権等: | © 2019. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ The full-text file will be made open to the public on 5 July 2020 in accordance with publisher's 'Terms and Conditions for Self-Archiving'. This is not the published version. Please cite only the published version. この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。 |
URI: | http://hdl.handle.net/2433/241701 |
DOI(出版社版): | 10.1016/j.bbrc.2019.05.055 |
PubMed ID: | 31097227 |
出現コレクション: | 学術雑誌掲載論文等 |
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