CD82は,脂質ラフトのクラスタリングとCD44の内皮細胞の密輸を変化させることで,病的な血管新生を抑制する

Quan Wei¹, Feng Zhang¹, Mekel M Richardson¹

¹From the West China Hospital, Sichuan University, Chengdu, China (Q.W.); University of Oklahoma Health Science Center, Oklahoma City (Q.W., F.Z., M.M.R., W.R., Y.L., C.F., Y.D., C.H., L.D., Y.H., J.M., X.A.Z.); University of Vermont, Burlington (N.H.R., M.T.); University of Tennessee, Memphis (W.Z., Y.C., Y.S.); Tongji Hospital, Wuhan, China (Y.D., X.H.); Indiana University, Indianapolis (M.E.B.); Oklahoma Medical Research Foundation, Oklahoma City (S.P., J.D.W.); and German Cancer Research Center, Heidelberg, Germany (S.T., G.J.H.).

Circulation

|August 24, 2014

まとめ

テトラスパニンCD82は,内皮細胞の動きを阻害することによって,病的な血管新生を抑制します. その欠如は細胞の移動と侵入を高め,血管新生に関連する疾患の潜在的治療標的を提供します.

科学分野:

血管生物学血管生物学
セルラー・シグナリング
分子医学は分子医学である.

背景:

血管新生は,がんや炎症などの疾患において不可欠です.
血管新生の内皮細胞 (EC) 調節は完全に理解されていません.
ECにおけるテトラスパニンCD82の血管作用は不明である.

研究の目的:

血管新生におけるCD82の機能を調査する.
CD82が内皮細胞の行動にどのように影響するかを決定する.
病理学的血管新生におけるCD82の役割を探求する.

主な方法:

Cd82-nullマウスの血管新生を,in vivoおよびex vivoアッセイを用いて調べました.
Cd82-null ECsにおける細胞機能,分子相互作用,シグナル伝達を分析した.
細胞粘着分子,脂質ラフト,エンドサイトーシスの変化を評価した.

主要な成果:

Cd82の消去により,血管新生反応が著しく増加した.
Cd82-null ECは,移住と侵略が増加したことを示した.
CD44とインテグリンのアップレギュレーション,脂質ラフトのクラスタリングの増加,およびエンドサイトーシスの変化が観察されました.

結論:

CD82は,ECの動きを制限することによって,病的な血管新生を抑制します.
脂質ラフト・クラスタリングと細胞粘着分子の密輸は,血管新生の可能性を調節する.
CD82-ギャングリオサイド-CD44信号調節は,病的な血管新生を弱める可能性があります.

キーワード:

細胞運動細胞の動きエンドキュトーシスエンドキュトーシス膜マイクロドメイン新血管化,病理学的新血管化

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