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. 2014 Sep 12;115(7):662-7.
doi: 10.1161/CIRCRESAHA.115.304634. Epub 2014 Jul 28.

Transdifferentiation of vascular smooth muscle cells to macrophage-like cells during atherogenesis

Susanne Feil  1 , Birgit Fehrenbacher  1 , Robert Lukowski  1 , Frank Essmann  1 , Klaus Schulze-Osthoff  1 , Martin Schaller  1 , Robert Feil  2
Affiliations

Transdifferentiation of vascular smooth muscle cells to macrophage-like cells during atherogenesis

Susanne Feil et al. Circ Res. .

Abstract

Rationale: Atherosclerosis is a widespread and devastating disease, but the origins of cells within atherosclerotic plaques are not well defined.

Objective: To investigate the specific contribution of vascular smooth muscle cells (SMCs) to atherosclerotic plaque formation by genetic inducible fate mapping in mice.

Methods and results: Vascular SMCs were genetically pulse-labeled using the tamoxifen-dependent Cre recombinase, CreER(T2), expressed from the endogenous SM22α locus combined with Cre-activatable reporter genes that were integrated into the ROSA26 locus. Mature SMCs in the arterial media were labeled by tamoxifen treatment of young apolipoprotein E-deficient mice before the development of atherosclerosis and then their fate was monitored in older atherosclerotic animals. We found that medial SMCs can undergo clonal expansion and convert to macrophage-like cells that have lost classic SMC marker expression and make up a major component of advanced atherosclerotic lesions.

Conclusions: This study provides strong in vivo evidence for smooth muscle-to-macrophage transdifferentiation and supports an important role of SMC plasticity in atherogenesis. Targeting this type of SMC phenotypic conversion might be a novel strategy for the treatment of atherosclerosis, as well as other diseases with a smooth muscle component.

Keywords: atherosclerosis; cell transdifferentiation; macrophages; muscle, smooth, vascular.

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