持続した心房細動中に心筋GRP94値の増加: 保護的反応?

M Vitadello¹, J Ausma, M Borgers

¹CNR Unit for Muscle Physiology and Physiopathology, Department of Biomedical Sciences, University of Padova, Padova, Italy.

Circulation

|May 23, 2001

まとめ

慢性心房細動は,心臓細胞におけるグルコース調節タンパク質GRP94の増加につながります. このGRP94の増加は逆行性であり,動性心房における保護性細胞応答を示唆する.

科学分野:

心血管生物学心血管生物学
細胞のストレス反応は,
分子心臓病学分子心臓病学

背景:

心房細動は,心筋細胞の構造的および現象的変化と関連しています.
グルコース調節タンパク質GRP94は細胞生存に不可欠であり,心房細動におけるその役割は不明である.

研究の目的:

慢性心房動中の心房心筋細胞におけるGRP94発現の変化を調査する.
動脈動のヒトおよび動物モデルにおいて,GRP94レベルが変化しているかどうかを判断する.

主な方法:

免疫学的アプローチを用いたヤギとヒトの心房筋内におけるGRP94発現の分析.
羊の心房細動の誘導と維持は,最大16週間,その後は心臓転換.
GRP94増加の位置を心筋細胞内で確認するために,免疫ヒストロケミカル分析.

主要な成果:

羊の心房筋細胞では,GRP94の濃度が4~16週間の動後に倍増し,心臓転換後に正常に戻った.
GRP94の上昇は,ヒトの動性心房サンプルでも観察されました.
カレティキュリンとは異なり,誘導性HSP70は動性心房で増加し,ストレス反応を示唆しました.

結論:

GRP94の有意で可逆的な増加は,慢性心房細動の間に心房筋細胞で発生します.
このGRP94のアップレギュレーションは,フィブリレーションへの応答として,保護的な細胞メカニズムを表している可能性があります.
この発見は,ストレスに対する心筋細胞の適応反応におけるGRP94の潜在的な役割を強調しています.

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