エストロゲンはAT1受容体の遺伝子発現をin vitroおよびin vivoで調節する
G Nickenig1, A T Bäumer, C Grohè
1Klinik III für Innere Medizin, Universität zu Köln, Germany. georg.nickenig@uni-koeln.de
Circulation
|June 19, 1998
まとめ
エストロゲン欠乏はAT1受容体の発現を増加させ,高血圧と動脈硬化に寄与する. エストロゲン置換療法は,この効果を逆転させ,心臓血管の健康に対する保護的役割を強調します.
科学分野:
- 心血管生物学 心血管生物学
- エンドクリノロジー エンドクリノロジー
- 分子医学は分子医学である.
背景:
- アンジオテンシンII型1 (AT1) 受容体は高血圧と動脈硬化に関与しています.
- エストロゲン欠乏は,心血管疾患のリスクの増加と関連しています.
研究 の 目的:
- 卵巣切除されたネズミのAT1受容体遺伝子発現に対するエストロゲン欠乏と置換の影響を調査する.
- 血管の滑らかな筋肉細胞におけるAT1受容体発現に対するエストロゲンの影響を決定する.
主な方法:
- エストロゲン補充療法を受けたり,受けなかったりした卵巣切除されたラットを研究した.
- アンジオテンシンII誘発の血管収縮,AT1受容体mRNAレベル (qPCR,Northern blotting) およびAT1受容体密度 (ラジオリンガンド結合) を評価した.
- また,培養された血管性滑らかな筋肉細胞でも実験を行った.
主要な成果:
- エストロゲン欠乏症は,ラットアオルタのAT1受容体密度 (160%) とmRNAレベル (187%) を著しく増加させた.
- エストロゲン置換療法により,AT1受容体の過剰発現が正常化しました.
- エストラディオールはAT1受容体mRNAをダウン調節し,培養された血管の滑らかな筋肉細胞における密度.
結論:
- エストロゲン欠乏はAT1受容体発現を上調し,高血圧と動脈硬化症との関連を説明する可能性がある.
- エストロゲンは,血管の滑らかな筋肉細胞におけるAT1受容体発現に直接的な抑制効果を発揮する.
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