C/EBPの転写因子は,心臓の発達と損傷の間に表心臓の活性化を媒介する
Guo N Huang1, Jeffrey E Thatcher, John McAnally
1Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Science (New York, N.Y.)
|November 20, 2012
まとめ
心臓の修復に不可欠な表皮は,損傷後の発達遺伝子を再活性化します. CCAAT/エンハンサー・バインディング・タンパク質 (C/EBP) 因子は,この表心臓遺伝子の活性化を制御し,心臓の再生のための新しい道を開きます.
科学分野:
- 心血管生物学 心血管生物学
- 発達生物学 発達生物学について
- 再生医学は,再生医療である.
背景:
- エピカルジウムは心臓の発達と修復に不可欠であり,前身細胞とシグナル分子を供給します.
- 大人の心臓損傷は,発達遺伝子プログラムの表心部再活性化を誘発するが,その基礎となる転写的調節は不明である.
研究 の 目的:
- 心臓発育および損傷中に表心臓遺伝子発現を制御する転写メカニズムを特定する.
- CCAAT/エンハンサー結合タンパク質 (C/EBP) 転写因子の表心臓活性化および心臓修復における役割を調査する.
主な方法:
- マウスの胚性心臓臓器培養と遺伝子発現システムを確立しました.
- 発達と損傷の間に活性化される同定された表心臓増強剤.
- これらの強化剤の調節におけるC/EBP転写因子の役割を分析した.
主要な成果:
- C/EBP因子を中心としたトランスクリプションコードを発見し,それは上心臓増強剤の活性化を制御する.
- C/EBPシグナル伝達が,心臓損傷中の上心部活性化に不可欠であることを実証した.
- 大人の上心部におけるC/EBPシグナル伝達を妨害することで,中性粒子の浸透を減少させ,傷害後の心臓機能を改善することが示された.
結論:
- CCAAT/エンハンサー・バインディング・タンパク質 (C/EBP) 転写因子は,心臓損傷への反応として表心部活性化のための転写的基礎を提供します.
- エピカルジウムにおけるC/EBPシグナリングをターゲットにすることで,心臓の再生を促進し,心臓損傷後の結果を改善するための潜在的な治療戦略を提示します.
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