Dataset Information

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^ΔLysMLdlr^-/-, neutrophil-specific Stat4^ΔS100A8Ldlr^-/-, and control Stat4^fl/flLdlr^-/- mice. All groups were fed a high-fat/cholesterol diet (HFD-C) for 28 weeks to establish advanced atherosclerosis. Aortic root plaque burden

SUBMITTER: Keeter WC

PROVIDER: S-EPMC10313069 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Dataset Information

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

Background and aims

Methods

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

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

Background and aims

Methods

OmicsDI is part of the ELIXIR infrastructure

Tweets

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