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レグマインはインテグリンαvβ3の内生変調子であり,血管退化,解剖,破裂を引き起こす

Lihong Pan^1,2,3, Peiyuan Bai^4,2,3, Xinyu Weng^4,2,3

¹Institutes of Biomedical Sciences, Fudan University, Shanghai, China (L.P., S.C., A.S., J.G.).

|January 31, 2022

まとめ

レグマイン (LGMN) は,血管の滑らかな筋肉細胞の変容を可能にすることで,胸部大動脈解剖 (TAD) を促進する. マクロファージのLGMNを阻害することは,TADの予防と治療のための新しい治療戦略を提供することができる.

科学分野:

心血管生物学
分子医学
血管生物学

背景:

胸腔大動脈解剖 (TAD) は,細胞外マトリックス分解と血管滑らかな筋肉細胞 (VSMC) のフェノタイプスイッチングを含む.
レグマイン (LGMN) は細胞外マトリックス分解に関与しているが,VSMCの分化とTADの病原性におけるその役割は不明である.

研究の目的:

VSMCの分化におけるLGMNの役割と,胸大動脈解剖 (TAD) に対するその貢献を調査する.

主な方法:

公的なマイクロアレイデータセットから差異的に発現した遺伝子をスクリーニングした.
Lgmnノックアウトマウス (マクロファージ特異性を含む) とBAPN誘発のTADモデルを使用した.
RNAシーケンシング,細胞コカルチャーアッセイ,共免疫プレシピテーション,およびコロカライゼーション分析を行った.

主要な成果:

LGMNはTAD患者とマウスの大動脈と血清で調節された.
Lgmn欠乏または抑制はTADの進行と細胞外マトリックス分解を改善しました.
マクロファージ由来のLGMNは,インテグリンαvβ3と相互作用し,TADを悪化させ,VSMCの分化を阻害した.

結論:

特にマクロファージからのLGMNシグナリングは,TADの発達において重要な役割を果たします.
LGMNをターゲットにすることで,胸前大動脈解剖の新たな治療戦略が生まれます.

キーワード:

GTPフォスフォヒドローラゼ動脈瘤,解剖する細胞外マトリックスインテグリン筋肉滑らか血管

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