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KAKEN_17K16129seika.pdf
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Title |
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β1インテグリン/RhoK介在性・新規血管内皮透過性制御機構の解明
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β1 インテグリン / RhoK カイザイセイ・シンキ ケッカン ナイヒ トウカセイ セイギョ キコウ ノ カイメイ
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β1 integurin / RhoK kaizaisei shinki kekkan naihi tōkasei seigyo kikō no kaimei
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Elucidation of novel beta 1 integrin-dependent mechanisms regulating vascular permeability
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伊澤, 良兼
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イザワ, ヨシカネ
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Izawa, Yoshikane
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慶應義塾大学・医学部 (信濃町)・講師
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Research team head
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科研費研究者番号 : 90468471
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髙橋, 愼一
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タカハシ, シンイチ
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Takahashi, Shin'ichi
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畝川, 美悠紀
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ウネカワ, ミユキ
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Unekawa, Miyuki
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塚田, 直己
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ツカダ, ナオキ
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Tsukada, Naoki
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2019
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科学研究費補助金研究成果報告書
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2018
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当研究は脳虚血モデルマウスを用い、血管透過性亢進メカニズムの解明を行った。虚血中心部においては、虚血後3時間以内に70kDa RITC dextranが血管外に漏出する可能性が示された。また、24時間の虚血暴露により、毛細血管だけでなく、径の大きい細小動脈においても血管透過性が亢進する様子が確認された。当研究と同時並行で行われた頭部MR (Myelin map) を用いた観察研究では、深部白質病変における髄鞘障害が確認された。過去の研究結果とあわせ、虚血が血管内皮細胞のβ1インテグリン介在性細胞内シグナルの変化を介して血管透過性を亢進させ、白質病変を含む実質障害を進行させる可能性が示された。
We investigated here the process of inducing increased permeability using a model mouse with permanent or transient ischemia, and examined whether white matter lesions in FLAIR or T2-weighted images in a human contain demyelination by a novel MR modality, Myelin-map, which can depict demyelination specifically. The results showed that microvascular permeability can increase in a few hours after the onset of ischemia, and 70kDa RITC dextran passed through the small vessels and capillaries in the ischemic core. Myelin-map showed demyelination in the white matter lesions in humans. These data suggested the possibility that leaked serum proteins, which have a molecular weight of around 70 kDa, might contribute to disruption of microvessels and damages of neuropil, observed after ischemia. These findings would provide a novel approach to the treatment of cerebral disorders including stroke and vascular dementia where the leaky vascular wall is relevant to their progression and complication.
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研究種目 : 若手研究(B)
研究期間 : 2017~2018
課題番号 : 17K16129
研究分野 : 脳血管障害
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