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Masharh Lipscomb¹, Sean Walis¹, Michael Marinello¹

¹Department of Molecular and Cellular Physiology, Albany Medical College, Albany, New York, USA.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|March 18, 2024

概括

通过激活GPR18在髓状细胞中,Resolvin D2 (RvD2) 限制了动脉样硬化. 这项研究表明RvD2

科学领域:

免疫学免疫学免疫学
心血管研究研究心血管研究
药理学药理学是指药理学的学科.

背景情况:

失调的炎症分辨率有助于动脉样硬化.
像Resolvin D2 (RvD2) 一样,Resolvins是炎症解决的关键媒介.
RvD2激活了GPR18,这是一种参与限制斑块进展的受体,但其细胞标是未知的.

研究的目的:

研究GPR18在动脉样硬化中的作用.
为了确定RvD2的动脉保护作用是否通过骨髓体GPR18.18进行介导.

主要方法:

开发出人性化的GPR18流体化 (fl/fl) 和骨髓细胞特异性的GPR18淘汰 (mKO) 鼠标.
在骨髓衍生巨细胞 (BMDMs) 中评估了细胞.
对Ldlr-/-接受者进行骨髓移植,并使用RvD2或载体进行治疗.

主要成果:

在fl/fl BMDMs中,RvD2增强了效细胞酶,但在mKO BMDMs中没有.
骨髓细胞GPR18缺乏导致斑块亡和亡的增加,并减少了细胞体的标志物.
在fl/fl接受者中,RvD2减少了斑块亡和亡,但在mKO接受者中没有.

结论:

骨髓细胞中的GPR18在限制动脉样硬化进展方面发挥着至关重要的作用.
RvD2的动脉保护作用,特别是减少斑块亡,部分取决于髓质GPR18.

关键词:

动脉样硬化动脉样硬化这是一种炎症炎症炎症炎症.巨细胞是一个巨细胞.骨髓化物骨髓化物解决方案的解决方案解决方案的解决方案.在这个问题上,我已经解决了.

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