Myeloid protein tyrosine phosphatase 1B (PTP1B) deficiency protects against atherosclerotic plaque formation in the ApoE^-/- mouse model of atherosclerosis with alterations in IL10/AMPKα pathway.

ABSTRACT:

Objective

Cardiovascular disease (CVD) is the most prevalent cause of mortality among patients with Type 1 or Type 2 diabetes, due to accelerated atherosclerosis. Recent evidence suggests a strong link between atherosclerosis and insulin resistance due to impaired insulin receptor (IR) signaling. Moreover, inflammatory cells, in particular macrophages, play a key role in pathogenesis of atherosclerosis and insulin resistance in humans. We hypothesized that inhibiting the activity of protein tyrosine phosphatase 1B (PTP1B), the major negative regulator of the IR, specifically in macrophages, would have beneficial anti-inflammatory effects and lead to protection against atherosclerosis and CVD.

Methods

We generated novel macrophage-specific PTP1B knockout mice on atherogenic b

SUBMITTER: Thompson D 

PROVIDER: S-EPMC5518727 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature