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緊張の異質性は,心筋壁の形状と運命を決定する
Rashmi Priya1,2, Srinivas Allanki3, Alessandra Gentile3
1Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany. rashmi.priya@crick.ac.uk.
Nature
|November 19, 2020
まとめ
発達中の心臓の局所的な緊張の違いが 細胞の運命を決定します 細胞の混雑は緊張を引き起こし 細胞が新しい層を形成し 適切な臓器の発達を保証します
科学分野:
- 発達生物学
- 細胞メカニズム
- 臓器生成
背景:
- 心臓の形成には極めて重要で, 異なるコンパクトとトラベキュラー層を形成する.
- 心臓のトラベキュレーションの欠陥は心筋病と胚の死亡につながる.
- トラベキュラー心筋細胞を特定するために組織対称性が破られるメカニズムは不明である.
研究 の 目的:
- 組織規模の力や細胞のメカニズムが 心臓のトラベキュレーション中に細胞の運命決定にどのように影響するかを調査する.
- トラベキュラー心筋細胞の特定における局所的な緊張異質性の役割を明らかにする.
- 臓器のパターンにおける 機械的な力と信号経路の相互作用を理解する
主な方法:
- 心臓の発達を研究するためのモデル生物としてゼブラフィッシュを使用した.
- 細胞の混雑とアクトミオシン収縮が心筋細胞の分層化に及ぼす影響を調査した.
- トラベキュレーション不足のゼブラフィッシュモデルで 遺伝子モザイクを使用した.
- ノッチ・レポーター表現を用いて心筋細胞の運命を評価した.
主要な成果:
- 増殖によって引き起こされる細胞の混雑によって引き起こされる局所的な緊張異質性は,心筋細胞の分層と状層の種を決定する.
- 細胞の混雑を増加させると 分層化が強化され,減少しるとそのプロセスが廃止される.
- アクトミオシンの収縮性を誘導すると,Nrg- Erbb2や血流のような上流信号がない場合でも,デラミネーションを救出し,心臓肌細胞の運命の特異化を促進します.
- ニッチ・シグナリングは,過剰なデラミネーションを制限し,心筋壁の構造を維持します.
結論:
- 組織規模の力は局所的な細胞力学に収束し,複雑な臓器形態を生成し,心臓のトラベキュレーション中に細胞運命を調節する.
- 機械的な力とシグナル伝達経路の間の多層面の制御相互作用は 頑丈で自己組織化された臓器のパターンを保証します
- これらのメカニズムを理解することで 心臓の先天性欠陥を防ぐことができます
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