Role of smooth muscle-derived S100A4 in an atherosclerotic mouse model

نویسندگان

چکیده

Abstract Background S100A4, a small calcium binding protein, plays an important role in vascular smooth muscle cell (SMC) phenotypic switch but its implication atherosclerotic plaque development and particularly SMC plasticity is not clear yet. By neutralizing S100A4 using monoclonal antibody, we have previously shown reduction overall burden. However, this strategy did distinguish the different contribution between SMCs or other S100A4-expressing cells (e.g. macrophages). Methods Herein, used lineage tracing mouse model which induced specific deletion of (SMC-S100A4Δ/Δ) ApoE−/− background. High cholesterol diet was maintained for 12 weeks, after which, SMC-S100A4Δ/Δ control mice (SMC-S100A4wt/wt) were sacrificed aortas processed staining single RNA sequencing (scRNA-seq). Results We showed that modulated composition rather than size. ScRNA-seq analysis from SMC-S100A4wt/wt macrophages dendritic increase total SMCs, likely participating fibrous cap stabilization. populations decrease macrophage-like inflammatory phenotype fibroblast-like repair phenotype, as well retention markers, namely Acta2 Myh11. Gene expression revealed inflammation fatty acid metabolism, extracellular matrix-related genes, classical markers maintenance contractile phenotype. Conclusion report intrinsic function establishment fate within and, surprisingly, global impact on microenvironnement status. Funding Acknowledgement Type funding sources: Public grant(s) – National budget only. Main source(s): Swiss Science Foundation

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ژورنال

عنوان ژورنال: European Heart Journal

سال: 2022

ISSN: ['2634-3916']

DOI: https://doi.org/10.1093/eurheartj/ehac544.3050