Origin and differentiation of vascular smooth muscle cells

Abstract

Vascular smooth muscle cells (SMCs), a major structural component of the vessel wall, not only play a key role in maintaining vascular structure but also perform various functions. During embryogenesis, SMC recruitment from their progenitors is an important step in the formation of the embryonic vascular system. SMCs in the arterial wall are mostly quiescent but can display a contractile phenotype in adults. Under pathophysiological conditions, i.e. vascular remodelling after endothelial dysfunction or damage, contractile SMCs found in the media switch to a secretory type, which will facilitate their ability to migrate to the intima and proliferate to contribute to neointimal lesions. However, recent evidence suggests that the mobilization and recruitment of abundant stem/progenitor cells present in the vessel wall are largely responsible for SMC accumulation in the intima during vascular remodelling such as neointimal hyperplasia and arteriosclerosis. Therefore, understanding the regulatory mechanisms that control SMC differentiation from vascular progenitors is essential for exploring therapeutic targets for potential clinical applications. In this article, we review the origin and differentiation of SMCs from stem/progenitor cells during cardiovascular development and in the adult, highlighting the environmental cues and signalling pathways that control phenotypic modulation within the vasculature.

Obesity Induces Artery-Specific Alterations: Evaluation of Vascular Function and Inflammatory and Smooth Muscle Phenotypic Markers

“…Endothelial and smooth muscle cells present different characteristics depending on the artery type, since the embryogenic origin and function of large conduit and small resistance arteries are different [18–20]. Thus, the impact of obesity could be different depending on the artery type, but in general studies evaluate a single artery type.…”

The transition of smooth muscle cells from a contractile to a migratory, phagocytic phenotype: direct demonstration of phenotypic modulation

“…; reviewed by Wang et al . ) and SMCs have been reported to be incapable of altering phenotype either in vitro or in vivo (Holifield et al . ; Tang et al .…”

Atherosclerosis-associated differentially methylated regions can reflect the disease phenotype and are often at enhancers

“…Among genes associated with athero hypermeth DMRs, there was a strong over-representation of atherosclerosis-relevant GO terms, including actin cytoskeleton organization, smooth muscle contraction, focal adhesion, cell death, and the TGFβ-receptor signaling pathway, which is related to SMC phenotypic switching [40]. ELN , which was associated with many athero hypermeth DMRs, encodes a major structural protein in aorta relevant to atherosclerosis (see Data in Brief Table 4 [15]).…”

“…TBX18 is implicated in the generation of SMCs during development [40] and was reported to be induced in the endothelial layer of atherosclerotic arteries [44]. NR2F2 is associated with phenotypic switching in vein endothelial cells [45].…”