アンドロゲン受容体は,心筋細胞における高縮を媒介する

J D Marsh¹, M H Lehmann, R H Ritchie

¹Department of Medicine, Harper Hospital, Detroit, Mich, USA. marsh@cardiology.harper.wayne.edu

Circulation

|August 11, 1998

まとめ

アンドロゲン受容体は,男女の心臓細胞に存在しています. これらの受容体は,アンドロゲンが心筋縮を直接引き起こし,心臓の機能に影響を及ぼすことを可能にします.

科学分野:

心臓病学心臓病学
分子生物学は分子生物学である.
エンドクリノロジーエンドクリノロジー

背景:

心筋細胞における心筋縮の原因となるアンドロゲンの直接的な役割は不明である.
この研究では,心臓のミオサイトがアンドロゲン受容体遺伝子を発現し,アンドロゲンに反応して過剰成長するかどうかを調べました.

研究の目的:

成人男性と女性の心筋細胞がアンドロゲン受容体遺伝子を発現しているかどうかを判断する.
心臓のミオサイトがアンドロゲンに反応し,高縮反応を示すかどうかをテストする.

主な方法:

アンドロゲン受容体トランスクリプトを検出するために,逆転写-ポリメラーゼ連鎖反応を利用した.
測定された [3H]フェニララニン組み込みと心房内ナトリウレチンペプチド分泌は,筋細胞縮の指標である.
ネズミ (成人,新生児),犬,ヒト (乳児,成人) のミオサイトを検査した.

主要な成果:

アンドロゲン受容体メッセンジャーRNAは,ヒトの心臓を含む種間の心筋細胞で検出されました.
テストステロンとジヒドロテストステロンの両方が,ミオサイトにおける有意な高縮性反応を誘発した.
ハイパルトロフィック反応は受容体特異的であり,タンパク質合成の増加と心房内ナトリウレチンペプチド分泌によって示された.

結論:

心筋細胞にはアンドロゲン受容体があり,アンドロゲンが心臓のフェノタイプに直接影響を及ぼし,高縮を引き起こします.
この発見は,アンドロゲンが心筋縮を調節する受容体媒介の直接的なメカニズムを示唆している.
人間におけるアンドロゲンの治療的または違法な使用に関して,臨床的意味合いがあります.

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