Endothelial cell CD36 mediates stroke-induced brain injury via BBB dysfunction and monocyte infiltration in normal and obese conditions.

ABSTRACT: CD36 expressed in multiple cell types regulates inflammation, vascular function, and innate immunity. Specifically, CD36 in microvascular endothelial cells (ECs) signals to elicit inflammation and causes EC death. This study investigated roles for EC-CD36 on acute stroke pathology in normal and obese conditions. Obesity induced by a high-fat diet (HD) selectively increased CD36 expression in ECs, not in monocytes/macrophages, in the post-ischemic brain. Mice deficient CD36 in ECs (EC^CD36-/-) showed reduced injury size and vascular permeability in normal conditions. While control mice fed a HD developed obesity and aggravated stroke injury, EC^CD36-/- mice were resistant to develop an obesity phenotype. Subjecting EC^CD36-/- mice to stroke resulted in reduced

SUBMITTER: Kim ID 

PROVIDER: S-EPMC10196754 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature