Blood flow mediates adipose tissue inflammation via endothelial cells.

血流通过内皮细胞介导脂肪组织炎症。

• 批准号: 22K08125
• 负责人: 匹田 貴夫
• 金额: $ 2.66万
• 依托单位: Okayama University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2022
• 资助国家: 日本
• 起止时间: 2022-04-01 至 2025-03-31
• 项目状态: 未结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22K08125/
• 关键词: 血管内皮細胞; 細胞極性; 炎症; メタボリックシンドローム; 機械学習; 流体力学; 組織間相互作用

メタボリックシンドロームモデルマウスにおけるPAR-3欠損の影響(1-2年目)初年度においては、初代培養血管内皮細胞に対してコントロールsiRNAまたはPard3 siRNAをトランスフェクションにより導入した。次に、これらの細胞を特殊なチャンバーに移し、層流または乱流を付加した条件下で培養した。現在、これらの培養細胞本体および培養上清を回収し、発現変動の認められる成長因子の解析を進めている。次に、予備実験として、野生型マウスを食餌誘導型メタボリックシンドロームモデルマウスとした。経時的に体重、血糖値および血中コレステロール量の変化を調べメタボリックシンドロームの進展に関わる基礎データを得た。また、同マウスより内臓脂肪および腎臓、肝臓を採取し、免疫細胞により血管内皮細胞のaxial polarityとマクロファージ浸潤の関連を解析している。さらに申請者は、組織における血管構造の最適化とその破綻による病態進展に着目し、研究を発展させている。血管新生の過程において、当初過剰に血管が形成された後に、プルーニングと呼ばれる不要な血管の刈り込みプロセスを経て、血管網の最適化が起こる。申請者らは、マウスの網膜血管網をモデルとし、免疫染色によりプルーニングされた血管を可視化し、機械学習モデルを用いてプルーニングサイトの予測モデルを確立した。今後、PAR-3ノックアウトマウスの血管網を用いて同様の解析を行い、血管内皮細胞の血流感受性が血管の成熟・リモデリングにおける役割を明らかにする。さらに、虚血により誘導される新生血管は病態の進展に重要な役割を果たす事が知られているが、PAR-3はこれら病的な新生血管の成熟に重要な役割を果たす可能性を検討する。

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