エストラディオールとプロゲスティンは,血管損傷後の白血球の浸透を差異的に調節します

Dongqi Xing¹, Andrew Miller, Lea Novak

¹Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, UAB Station, Birmingham, AL 35294, USA. dqxing@uab.edu

Circulation

|December 31, 2003

まとめ

エストロゲン (E2) は,小胞細胞のような炎症性細胞の移動を,ラットの損傷した動脈に減少させます. メドロキシプロゲステロンアセテート (MPA) は,この保護効果を阻害し,E2を強調します.

科学分野:

血管生物学血管生物学
エンドクリノロジーエンドクリノロジー
免疫学免疫学とは

背景:

血管損傷に対する反応において,炎症は極めて重要です.
エストロゲン (17β-エストラディオール,E2) はネオインティマの形成を阻害する.
メドロキシプロゲステロンアセテート (MPA) は,E2の抑制効果を逆行する.

研究の目的:

E2がラットの頸動脈に損傷後の炎症性細胞の移行を阻害するかどうかを調査する.
MPAがE2の炎症性細胞移動に対する効果を阻害するかどうかを判断する.

主な方法:

卵巣切除を受けたネズミは,E2,MPA,E2+MPA,または車両を受け,その後は風船による大動脈損傷を受けた.
炎症性細胞集団 (グラヌロサイト,モノサイト/マクロファージ,Tリンパ球) は,損傷後1,3,7日目にフローサイトメトリで定量化されました.
免疫ヒストケミストリーは,細胞の局所化を確認した.

主要な成果:

損傷した動脈は,対照群と比較して,粒細胞,単細胞/マクロファージ,Tリンパ球の有意な増加を示した.
E2治療は,粒細胞と単細胞/マクロファージの個体数を約50%減少させ,Tリンパ球を増加させた.
MPAは単独では効果がなかったが,炎症細胞に対するE2の抑制作用を完全に阻害した.

結論:

E2は,損傷した血管への白血球の侵入を減らすことにより,ネオインティマルの応答を制限する可能性があります.
アドベンチアル/ペリアドベンチアル組織からの白血球の移住は,重要な早期イベントです.
MPAは,血管損傷に対するエストロゲンの保護機構に干渉します.

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