Siglec-E retards atherosclerosis by inhibiting CD36-mediated foam cell formation.

ABSTRACT:

Background

The accumulation of lipid-laden macrophages, foam cells, within sub-endothelial intima is a key feature of early atherosclerosis. Siglec-E, a mouse orthologue of human Siglec-9, is a sialic acid binding lectin predominantly expressed on the surface of myeloid cells to transduce inhibitory signal via recruitment of SH2-domain containing protein tyrosine phosphatase SHP-1/2 upon binding to its sialoglycan ligands. Whether Siglec-E expression on macrophages impacts foam cell formation and atherosclerosis remains to be established.

Methods

ApoE-deficient (apoE^-/-) and apoE/Siglec-E-double deficient (apoE^-/-/Siglec-E^-/-) mice were placed on high fat diet for 3 months and their lipid profiles and severities of atherosclerosis were assess

SUBMITTER: Hsu YW 

PROVIDER: S-EPMC7784283 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature