細胞核は,組織損傷による炎症のメカニカルトランスデューサーとして機能する
Balázs Enyedi1, Mark Jelcic1, Philipp Niethammer1
1Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Cell
|May 21, 2016
まとめ
組織損傷は細胞の腫れを誘発し,核包膜の緊張を通してフォスフォリファースA2 (cPLA2) を活性化します. このプロセスは,アラキドン酸 (AA) を放出し,炎症誘発信号を生成することで炎症を誘発します.
科学分野:
- 細胞生物学
- 炎症に関する研究
- 機械生物学
背景:
- 組織損傷は炎症反応を引き起こします
- サイトソリックフォスホリファーゼA2 (cPLA2) はアラキドン酸 (AA) を放出し,エコサノイドを産生する.
- cPLA2を活性化させるための組織損傷を感知するメカニズムは不明です.
研究 の 目的:
- 組織損傷がcPLA2を活性化するメカニズムを解明する.
- 炎症時のメカニカルストレスを感知する核の役割を調査する.
主な方法:
- 負傷したゼブラフィッシュの幼虫の生写真です
- オスモティック細胞と核の腫れに対する cPLA2 転位を調査する.
- 隔離された核でcPLA2の転位を再構成する.
主要な成果:
- 傷はオスモティック細胞の腫れと イコサノイド信号の生成を引き起こします
- 細胞と核のオスモティック腫れは,核封筒への転移によってcPLA2を活性化します.
- 核の膨張は,Ca2+の上昇だけでなく,cPLA2の転位に不可欠です.
- cPLA2の転位は核膜の緊張によって引き起こされる物理的プロセスです.
結論:
- 核は炎症におけるメカノセンサとして機能する.
- 細胞の腫れと溶解は 炎症性イコサノイド信号に変換されます
- 核膜の緊張は,組織損傷後のcPLA2の活性化を媒介する.
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