Annexin A1 counteracts chemokine-induced arterial myeloid cell recruitment.

ABSTRACT:

Rationale

Chemokine-controlled arterial leukocyte recruitment is a crucial process in atherosclerosis. Formyl peptide receptor 2 (FPR2) is a chemoattractant receptor that recognizes proinflammatory and proresolving ligands. The contribution of FPR2 and its proresolving ligand annexin A1 to atherosclerotic lesion formation is largely undefined.

Objective

Because of the ambivalence of FPR2 ligands, we here investigate the role of FPR2 and its resolving ligand annexin A1 in atherogenesis.

Methods and results

Deletion of FPR2 or its ligand annexin A1 enhances atherosclerotic lesion formation, arterial myeloid cell adhesion, and recruitment. Mechanistically, we identify annexin A1 as an endogenous inhibitor of integrin activation evoked by the chemokines CCL5, CCL2, and CX

SUBMITTER: Drechsler M 

PROVIDER: S-EPMC7751381 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature