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在小鼠中向删除循环氧化酶-2和动脉动脉生成

Yiqun Hui¹, Emanuela Ricciotti, Irene Crichton

¹School of Medicine, Institute for Translational Medicine and Therapeutics, University of Pennsylvania, 153 Johnson Pavilion, Philadelphia, PA 19104, USA.

|June 10, 2010

概括

巨细胞循环氧化酶-2 (COX-2) 促进动脉样硬化,而T细胞COX-2不会影响其发展. 巨细胞中COX-2的缺失通过改变前列腺素的形状来减弱动脉生成.

科学领域:

心血管生物学心血管生物学
炎症研究炎症研究
动脉样硬化病原体的产生

背景情况:

血管循环氧化酶-2 (COX-2) 产生前环素 (PGI(2)),这通常会抑制动脉生成.
之前在动脉样硬化模型中对COX-2抑制和删除的研究产生了相互矛盾的结果.
这项研究旨在澄清COX-2在巨细胞和T细胞中的独特细胞作用.

研究的目的:

调查巨细胞衍生和T细胞衍生COX-2对动脉样硬化发展的具体贡献.
阐明不同细胞类型中COX-2影响炎症途径和疾病进展的机制.

主要方法:

使用LysMCre小鼠生成巨细胞特定的COX-2淘汰 (Mac-COX-2KOs).
使用CD4Cre小鼠创建了T细胞特异性COX-2淘汰 (TCKO).
在低密度脂蛋白受体淘汰赛小鼠模型中评估了前列腺素 (PG) 形成,COX-2表达和动脉动脉生成.

主要成果:

巨-COX-2删除抑制了脂多糖刺激的PG形成和全身PG生物合成.
在Mac-COX-2KOs交叉到超脂性模型中,动脉生成被减弱.
巨细胞COX-2的删除导致非白细胞血管细胞中COX-2表达的增加,这表明PG特征的转变.
T细胞COX-2删除没有影响PG生物合成,T细胞组成或动脉生成.

结论:

巨-COX-2,产生血栓素A(2) 和前列腺素E(2),促进动脉动脉生成.
大菌COX-2抑制了COX-2在损伤细胞中的表达,潜在的血管光滑肌肉细胞,它们产生体保护性前环素.
T细胞COX-2在T细胞发育,功能或小鼠动脉动脉生成中没有显著作用.

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