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Updated: Jun 30, 2026
12:43
On-Chip Endothelial Inflammatory Phenotyping
Published on: July 22, 2012
アンジオテンシンIIは,ヒトの血管内皮細胞による細胞間粘着分子-1 (ICAM-1) の発現を刺激し,溶解性ICAM-1の放出をin vivoで増加させます
L Pastore1, A Tessitore, S Martinotti
1University of L'Aquila, Department of Experimental Medicine, Rome, Italy.
Circulation
|October 12, 1999
まとめ
アンジオテンシンII (Ang II) は,内皮細胞における細胞間粘着分子-1 (ICAM-1) の発現および溶解性ICAM-1レベルを増加させます. カンデサルタンまたはロサルタンでAT(1) 受容体をブロックすると,これらのAng II誘発的効果が効果的に抑制されます.
科学分野:
- 心血管生物学 心血管生物学
- 内皮細胞生物学 内皮細胞生物学
- 高血圧の研究 高血圧の研究
背景:
- アンジオテンシンII (Ang II) は血管炎症に関与しています.
- 細胞間粘着分子-1 (ICAM-1) は,内皮機能不全に起因する.
研究 の 目的:
- ヒト静脈内皮細胞 (HUVEC) のICAM-1発現に対するAng IIの効果を調査する.
- 血溶性ICAM-1濃度に対するAng IIの影響を in vivoで決定する.
- これらの効果を媒介するAT(1) とAT(2) 受容体の役割を評価する.
主な方法:
- HUVECは,Ang IIおよび受容体阻害剤 (カンデサタン,PD12319) でインキュベートされました.
- ICAM-1 mRNA発現は,Northern blot.によって分析されました.
- 溶性ICAM-1放出はELISAで測定した.
- Ang IIは,ロサルタンまたはアテノロールの治療と併用または併用せずに,正常血圧および高血圧の個人に注入されました.
主要な成果:
- Ang IIはHUVECsでICAM-1 mRNAと溶解性ICAM-1の放出を著しく増加させました.
- Ang II輸液は,正常血圧と高血圧の両方の被験者において,血溶性ICAM-1レベルを上昇させた.
- カンデサルタンは,HUVECにおけるAng II誘発ICAM-1発現を阻害した.
- ロサルタンは,ベースラインの溶解性ICAM-1を低下させ,Ang II誘発のインクリメントを vivoで弱めた.
結論:
- Ang IIは,内皮細胞におけるICAM-1発現を上調する.
- Ang IIは,溶解性ICAM-1の放出をインビトロおよびインビボの両方で刺激する.
- AT(1) 受容体のブロックは,Ang II.の内皮効果を効果的に阻害する.
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