Deletion of Talin1 in Myeloid Cells Facilitates Atherosclerosis in Mice.

ABSTRACT:

Background

Integrin-regulated monocyte recruitment and cellular responses of monocyte-derived macrophages are critical for the pathogenesis of atherosclerosis. In the canonical model, talin1 controls ligand binding to integrins, a prerequisite for integrins to mediate leukocyte recruitment and induce immune responses. However, the role of talin1 in the development of atherosclerosis has not been studied. Our study investigated how talin1 in myeloid cells regulates the progression of atherosclerosis.

Methods

On an Apoe^-/- background, myeloid talin1-deficient mice and the control mice were fed with a high-fat diet for 8 or 12 weeks to induce atherosclerosis. The atherosclerosis development in the aorta and monocyte recruitment into atherosclerotic lesi

SUBMITTER: Shi H 

PROVIDER: S-EPMC12695087 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature