著者
松田 道行 今村 健志 清川 悦子 宮脇 敦史 根本 知己 岡田 峰陽 石井 優 福原 茂朋
出版者
京都大学
雑誌
新学術領域研究(研究領域提案型)
巻号頁・発行日
2010-04-01

平成26年度までの計画班員および公募班員の研究報告書を取りまとめ、編集作業を行った後、評価報告書を作成し、関係者に送付した。また、研究終了後も要望の強いDNAの配布や技術講習会も開催した。さらに、Web情報の更新も行った。平成27年度に新しい新学術領域研究「レゾナンスバイオ」が始まったので、この領域への情報の引き継ぎを行った。
著者
福原 茂朋 望月 直樹
出版者
公益社団法人 日本薬学会
雑誌
YAKUGAKU ZASSHI (ISSN:00316903)
巻号頁・発行日
vol.130, no.11, pp.1413-1420, 2010 (Released:2010-11-01)
参考文献数
20
被引用文献数
3 3

Endothelial cells lining blood vessels are in tight contact with each other, thereby maintaining vascular integrity. Compromising vascular integrity leads to an increase in vascular permeability, which is associated with chronic inflammation, edema, and tumor angiogenesis. Vascular endothelial (VE)-cadherin is an endothelium-specific cell-cell adhesion molecule involved in endothelial barrier functions. We previously reported that cyclic AMP-elevating agonists such as prostaglandins and adrenomedullin potentiate VE-cadherin-dependent cell adhesion by inducing activation of Rap1 small GTPase through Epac. We further investigated the mechanism whereby Rap1 potentiates VE-cadherin-dependent cell adhesion, and found that Rap1 induces the formation of circumferential actin bundles along the cell-cell junctions. Although it has been believed that α-/β-catenins anchor cadherin to the actin cytoskeleton to stabilize cadherin at cell-cell junctions (classical model), Nelson's and Weis' groups have recently suggested a new dynamic model in which α-/β-catenins do not stably connect actin to cadherin. However, our study clearly indicated that the circumferential actin bundles anchor VE-cadherin to the cell-cell junctions through α-/β-catenins. Thus Rap1 potentiates endothelial cell-cell junctions through the mechanism based on the static model.