Neutrophil-specific STAT4 deficiency attenuates atherosclerotic burden and improves plaque stability via reduction in neutrophil activation and recruitment into aortas of Ldlr ^-/- mice.

ABSTRACT:

Background and aims

Neutrophils drive atheroprogression and directly contribute to plaque instability. We recently identified signal transducer and activator of transcription 4 (STAT4) as a critical component for bacterial host defense in neutrophils. The STAT4-dependent functions of neutrophils in atherogenesis are unknown. Therefore, we investigated a contributory role of STAT4 in neutrophils during advanced atherosclerosis.

Methods

We generated myeloid-specific Stat4 ^ΔLysM Ldlr ^-/- , neutrophil-specific Stat4 ^ΔS100A8 Ldlr ^-/- , and control Stat4 ^fl/fl Ldlr ^-/- mice. All groups were fed a high-fat/cholesterol diet (HFD-C) for

SUBMITTER: Keeter WC 

PROVIDER: S-EPMC9980123 | biostudies-literature | 2023 Feb

REPOSITORIES: biostudies-literature