Impaired integrin β3 delays endothelial cell regeneration and contributes to arteriovenous graft failure in mice.

ABSTRACT:

Objective

Neointima formation is associated with stenosis and subsequent thrombosis in arteriovenous grafts (AVGs). A role of integrin β3 in the neointima formation of AVGs remains poorly understood.

Approach and results

In integrin β3(-/-) mice, we found significantly accelerated occlusion of AVGs compared with the wild-type mice. This is caused by the development of neointima and lack of endothelial regeneration. The latter is a direct consequence of impaired functions of circulating angiogenic cells (CACs) and platelets in integrin β3(-/-) mice. Evidence suggests the involvement of platelet regulating CAC homing to and differentiation at graft sites via transforming growth factor-β1 and Notch signaling pathway. First, CACs deficient of integrin β3 impaired adhesion activi

SUBMITTER: Liang M 

PROVIDER: S-EPMC4671198 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature