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May 3, 2018Arteriosclerosis Thrombosis and Vascular BiologyOpen Access

Myeloid β-Catenin Deficiency Exacerbates Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice

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Authors

FWFang WangAnhui Provincial Hospital ZLZun LiuNorthwestern Polytechnical University SPSehyung ParkUniversity of Kentucky

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Implication

Preclinical study reveals increased aortic atherosclerotic lesion areas in myeloid beta-catenin-deficient mice, indicating a protective anti-inflammatory role.

Key Points

To investigate how myeloid-specific β-catenin expression affects macrophage cellular function and the development of atherosclerotic plaques.
Generated low-density lipoprotein receptor-deficient mice harboring myeloid-specific β-catenin deletion (β-catenin Δmye LDLR−/−).
Assessed in vitro macrophage migration and adhesion, and measured aortic root atherosclerotic lesion size, plasma lipids, and plaque morphology in vivo.
Investigated downstream macrophage inflammatory pathways with a focus on signal transducer and activator of transcription (STAT) signaling.
Deletion of β-catenin impaired macrophage adhesion and migration properties in vitro.
Ablation of myeloid β-catenin significantly increased atherosclerotic lesion area in the aortic root without altering plasma lipid concentrations or plaque cellular composition.
Loss of β-catenin led to STAT3 downregulation and STAT1 activation, thereby elevating macrophage inflammatory responses and driving atherosclerosis progression.

Cite This Study

Wang et al. (2018) studied this question.

synapsesocial.com/papers/6a8a6a730e1a8f7244fd76eb https://doi.org/10.1161/atvbaha.118.311059

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