bcl-2遺伝子製品は,心室内髄細胞のプログラム細胞死を防ぐ
L A Kirshenbaum1, D de Moissac
1Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada. Lorrie@SBRC.umanitoba.ca
Circulation
|October 7, 1997
まとめ
抗アポプトシスタンパク質bcl-2は,p53.3によって誘発される心筋細胞のプログラム細胞死を防ぐ. この研究は,bcl-2を証明しています.
科学分野:
- 心血管生物学 心血管生物学
- 分子生物学は分子生物学である.
- 細胞死研究 細胞死の研究
背景:
- プログラムされた細胞死 (アポプトーシス) は,心臓筋において極めて重要です.
- p53は,さまざまな細胞タイプにおけるアポトーシスの誘発因子として知られています.
- 心臓のミオサイトアポトーシスの予防におけるbcl-2の役割は,調査が必要です.
研究 の 目的:
- 抗アポプトシスタンパク質bcl-2が,心筋細胞 (心室筋細胞) のp53誘発のアポプトシスを予防できるかどうかを判断する.
主な方法:
- 複製に欠陥のあるアデノウイルスを利用して,bcl-2とp53遺伝子を心室筋細胞に届けました.
- 生命染色を用いた肌細胞細胞死亡を評価した.
- DNAの断片化と末端移転酵素デオキシヌクレオチドの末端ラベリングによるアポプトシスの評価.
- バックスプロモーターの転写レベルを測定した.
主要な成果:
- p53は,心室筋細胞死亡とアポトーシスを有意に増加させた.
- また,p53はバックスプロモーターの転写を増加させた.
- bcl-2発現は,p53-誘発の肌細胞死とアポトーシスを防止しました.
- bcl-2はp53-依存バックス転写を抑制した.
結論:
- bcl-2は,心室筋細胞における抗アポプトシス因子として機能する.
- これは,BCL-2が心筋細胞における抗アポプトティック作用を示す最初の証拠である.
- bcl-2の保護効果は,p53媒介のバックス転写の抑制と関連しています.
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