The Role of Smooth Myocytes and Macrophages in Development of Complicated Forms of Arterial Atherosclerosis

Purpose:to conduct morphohistochemical and immunohistochemical study of arterial unstable atherosclerotic plaques for assessment of the state of smooth muscle cells (SMC) and macrophages.Materials and methods.The surgical material of the peripheral arteries (femoral, popliteal, external carotid) was obtained from 50 patients aged over 60 years, followed by morphohistochemical, immunohistochemical studies.Results.Hyperplasia of secretory smooth muscle cells (SMC), and new formation of thin-walled capillary vessels was noted in unstable atherosclerotic plaques. Macrophagic infiltration was detected in the intima of arteries, in places of accumulation of foam cells.Conclusion.Unstable atherosclerotic plaque is a cellular-intercellular process with the participation of lipids, macrophages, and with predominance of SMC and newly formed vessels.

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The role of smooth muscle cells in calcification of atherosclerotic plaques

10.26481/dis.20211207ts ◽

2021 ◽

Author(s):

Till Seime

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Atherosclerotic Plaques

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Neutralization of S100A4 induces stabilization of atherosclerotic plaques: role of smooth muscle cells

Atherosclerosis ◽

10.1016/j.atherosclerosis.2020.10.069 ◽

2020 ◽

Vol 315 ◽

pp. e18-e19

Author(s):

A. Sakic ◽

C. Chaabane ◽

N. Ambartsumian ◽

J. Klingelhöfer ◽

S. Lemeille ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Atherosclerotic Plaques

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Neutralization of S100A4 induces stabilization of atherosclerotic plaques: role of smooth muscle cells

Cardiovascular Research ◽

10.1093/cvr/cvaa311 ◽

2020 ◽

Author(s):

A Sakic ◽

C Chaabane ◽

N Ambartsumian ◽

J Klingelhöfer ◽

S Lemeille ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Smooth Muscle Actin ◽

Muscle Cells ◽

Atherosclerotic Plaques ◽

Porcine Coronary Artery ◽

Phenotypic Transition ◽

Synthetic Phenotype

Abstract Aims During atherosclerosis, smooth muscle cells (SMCs) accumulate in the intima where they switch from a contractile to a synthetic phenotype. From porcine coronary artery, we isolated spindle-shaped (S) SMCs exhibiting features of the contractile phenotype and rhomboid (R) SMCs typical of the synthetic phenotype. S100A4 was identified as a marker of R-SMCs in vitro and intimal SMCs, in pig and man. S100A4 exhibits intra- and extracellular functions. In this study, we investigated the role of extracellular S100A4 in SMC phenotypic transition. Methods and Results S-SMCs were treated with oligomeric recombinant S100A4 (oS100A4), which induced nuclear factor (NF)-κB activation. Treatment of S-SMCs with oS100A4 in combination with platelet-derived growth factor (PDGF)-BB induced a complete SMC transition toward a pro-inflammatory R-phenotype associated with NF-κB activation, through toll-like receptor-4. RNA sequencing of cells treated with oS100A4/PDGF-BB revealed a strong upregulation of pro-inflammatory genes and enrichment of transcription factor binding sites essential for SMC phenotypic transition. In a mouse model of established atherosclerosis, neutralization of extracellular S100A4 decreased area of atherosclerotic lesions, necrotic core, and CD68 expression and increased α-smooth muscle actin and smooth muscle myosin heavy chain expression. Conclusion We suggest that the neutralization of extracellular S100A4 promotes the stabilization of atherosclerotic plaques. Extracellular S100A4 could be a new target to influence the evolution of atherosclerotic plaques. Translational perspective Our studies indicate that extracellular S100A4 is causally related to atherosclerotic plaque progression putting it forward as a prospective therapeutic target for plaque stabilization and/or regression.

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