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演題詳細

Poster

アルツハイマー病、他の認知症、老化
Alzheimer's Disease, Other Dementia, Aging

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

周皮細胞におけるBMP-4の発現は白質障害と相関する
BMP-4 expression by immature pericytes correlates with white matter damage

  • P2-290
  • 上村 麻衣子 / Maiko Uemura:1 猪原 匡史 / Masafumi Ihara:3 中込 隆之 / Takayuki Nakagomi:4 松山 知弘 / Tomohiro Matsuyama:4 木下 彩栄 / Ayae Kinoshita:2 高橋 良輔 / Ryosuke Takahashi:1 
  • 1:京都大・医・神経内科 / Depertment of Neurology, Kyoto University Graduate School of Medicine 2:京都大・医・人間健康科学 / School of Human Health Sci, Univ of Kyoto, Kyoto, Japan 3:国立循環器病セ / Dept of Stroke and Cerebrovas Dis, National Cerebral and Cardiovascular Center Hospital, Osaka, Japan 4:兵庫医科大・神経再生 / Ins for Adv Med Sci, Hyogo College of Med, Hyogo, Japan 

BMP-4 expression by immature pericytes correlates with white matter damage.

Maiko Uemura 1,2, Masafumi Ihara3, Takayuki Nakagomi4, Tomohiro Matsuyama4, Ayae Kinoshita2, Ryosuke Takahashi1

1 Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
2 School of Human Health Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan
3 Department of Stroke and Cerebrovascular Diseases, National Cerebral and Cardiovascular Center Hospital, Osaka, Japan
4 Institute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo, Japan

[Introduction]
Signaling abnormalities in transforming growth factor β 1 (TGFβ1) play a detrimental role in CARASIL, a hereditary vascular cognitive impairment (VCI), and its superfamily members, bone morphogenic proteins (BMPs), are known to contribute to pro-atherogenesis and suppress oligodendrocyte progenitor cell (OPC). However, a comprehensive pathological analysis of BMPs in VCI has not been conducted.
[Methods]
We evaluated post-mortem frontal lobe tissue from 7 VCI, 6 Alzheimer's disease, and 6 age-matched disease controls. Brain sections were immunostained for TGFβ1, BMP-2, BMP-4, BMP-6, BMP-7, and BMP-9, and platelet derived growth factor receptor β (PDGFRβ) and α smooth muscle actin (αSMA) as pericyte markers, and PDGFRα as OPC marker.
[Results]
The expression of BMP-4 was significantly upregulated in the white matter of VCI, and colocalized with PDGFRβ than αSMA. The degree of myelin loss was correlated with greater expression of BMP-4. The number of OPC is decreased when BMP-4 expression was above a certain level.
[Conclusions]
Our findings suggest that myelin loss evolves in parallel with BMP-4 upregulation in immature pericytes, and above a certain level of BMP-4 expression is correlated with decreased OPC differentiation. Regulation of BMP-4 signaling has the potential as treatment strategy for VCI.

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