Sam68 impedes the recovery of arterial injury by augmenting inflammatory response.

ABSTRACT: OBJECTIVE:The role of Src-associated-in-mitosis-68-kDa (Sam68) in cardiovascular biology has not been studied. A recent report suggests that Sam68 promotes TNF-α-induced NF-κB activation in fibroblasts. Here we sought to dissect the molecular mechanism by which Sam68 regulates NF-κB signaling and its functional significance in vascular injury. APPROACH AND RESULTS:The endothelial denudation injury was induced in the carotid artery of Sam68-null (Sam68^-/-) and WT mice. Sam68^-/- mice displayed an accelerated re-endothelialization and attenuated neointima hyperplasia, which was associated with a reduced macrophage infiltration and lowered expression of pro-inflammatory cytokines in the injured vessels. Remarkably, the ameliorated vascular remodeling was recapitulated in

SUBMITTER: Han S 

PROVIDER: S-EPMC6889069 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature