A2bアデノシン受容体は,高脂血症と動脈硬化症を調節する
Milka Koupenova1, Hillary Johnston-Cox, Alexander Vezeridis
1Department of Medicine, Boston University School of Medicine, 700 Albany St, CVI, W-601, Boston, MA 02118, USA.
Circulation
|December 7, 2011
まとめ
A(2b) アデノシン受容体 (A(2b) ARは,肝臓の脂質代謝と動脈硬化を調節する. この受容体の活性化により,高脂血症および関連する心血管疾患に対する新しい治療戦略が提供される可能性があります.
科学分野:
- 心血管科学 心血管科学
- メタボリック疾患の研究
- 薬理学 薬理学とは
背景:
- cAMPを上昇させるアデノシン受容体 (A(2b) アデノシン受容体 (A(2b) AR) は,骨髄細胞を通して炎症に作用する.
- 代謝疾患と動脈硬化症におけるその特定の役割は,以前は不明でした.
研究 の 目的:
- ダイエット誘発性高脂血症および動脈硬化症におけるA(2b) ARの役割を調査する.
- A(2b) ARが肝臓の脂質代謝に影響を与える分子機構を決定する.
主な方法:
- アポリポプロテインE欠乏症のマウスは,動脈硬化症をモデル化するために高脂肪食を与えられた.
- 骨髄移植,肝臓の遺伝子/タンパク質発現分析 (ウエスタン・ブラッティング,qPCR),および原発性肝細胞研究を行いました.
- アデノウイルスの遺伝子配送と薬理学的なA(2b) ARアゴニスト/アンタゴニストが使用されています.
主要な成果:
- A(2b) AR欠乏症は動脈硬化症を悪化させ,肝臓/血のコレステロールとトリグリセリドの上昇を引き起こし,脂肪肝の病理学をもたらした.
- A(2b) AR欠乏症は,ステロール調節要素結合タンパク質-1 (SREBP-1) とリポゲン酵素の肝臓発現を増加させる.
- 肝臓にA(2b) ARを回復させるか,A(2b) ARアゴニストを投与することで,高脂血症と動脈硬化症が軽減されます.
結論:
- A(2b) ARは,肝臓のSREBP-1,高脂血症,動脈硬化症の重要な調節剤である.
- A(2b) ARをターゲットにすることは,代謝および心血管疾患に対する潜在的な治療戦略です.
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