Contribution of Vascular Cells to Neointimal Formation

PLoS One. 2017 Jan 6;12(1):e0168914. doi: 10.1371/journal.pone.0168914. eCollection 2017.

Abstract

The de-differentiation and proliferation of smooth muscle cells (SMCs) are widely accepted as the major contributor to vascular remodeling. However, recent studies indicate that vascular stem cells (VSCs) also play an important role, but their relative contribution remains to be elucidated. In this study, we used genetic lineage tracing approach to further investigate the contribution of SMCs and VSCs to neointimal thickening in response to endothelium denudation injury or artery ligation. In vitro and in vivo analysis of MYH11-cre/Rosa-loxP-RFP mouse artery showed that SMCs proliferated at a much slower rate than non-SMCs. Upon denudation or ligation injury, two distinct types of neointima were identified: Type-I neointimal cells mainly involved SMCs, while Type II mainly involved non-SMCs. Using Sox10-cre/Rosa-loxP-LacZ mice, we found that Sox10+ cells were one of the cell sources in neointima. In addition, lineage tracing using Tie2-cre/Rosa-LoxP-RFP showed that endothelial cells also contributed to the neointimal formation, but rarely transdifferentiated into mesenchymal lineages. These results provide a novel insight into the contribution of vascular cells to neointima formation, and have significant impact on the development of more effective therapies that target specific vascular cell types.

MeSH terms

  • Actins / metabolism
  • Animals
  • Biomarkers
  • Carotid Arteries / cytology
  • Carotid Arteries / metabolism
  • Carotid Arteries / pathology
  • Carotid Artery Injuries / etiology
  • Carotid Artery Injuries / metabolism
  • Carotid Artery Injuries / pathology
  • Cell Transdifferentiation
  • Disease Models, Animal
  • Endothelial Cells / cytology
  • Endothelial Cells / metabolism*
  • Endothelial Cells / pathology
  • Female
  • Gene Expression
  • Genes, Reporter
  • Male
  • Mice
  • Mice, Transgenic
  • Muscle, Smooth, Vascular
  • Myocytes, Smooth Muscle / metabolism
  • Neointima / etiology*
  • Neointima / metabolism*
  • Neointima / pathology
  • SOXE Transcription Factors / metabolism

Substances

  • Acta2 protein, mouse
  • Actins
  • Biomarkers
  • SOXE Transcription Factors
  • Sox10 protein, mouse