Adventitial Sca1+ Cells Transduced With ETV2 Are Committed to the Endothelial Fate and Improve Vascular Remodeling After Injury

Arterioscler Thromb Vasc Biol. 2018 Jan;38(1):232-244. doi: 10.1161/ATVBAHA.117.309853. Epub 2017 Nov 30.

Abstract

Objective: Vascular adventitial Sca1+ (stem cell antigen-1) progenitor cells preferentially differentiate into smooth muscle cells, which contribute to vascular remodeling and neointima formation in vessel grafts. Therefore, directing the differentiation of Sca1+ cells toward the endothelial lineage could represent a new therapeutic strategy against vascular disease.

Approach and results: We thus developed a fast, reproducible protocol based on the single-gene transfer of ETV2 (ETS variant 2) to differentiate Sca1+ cells toward the endothelial fate and studied the effect of cell conversion on vascular hyperplasia in a model of endothelial injury. After ETV2 transduction, Sca1+ adventitial cells presented a significant increase in the expression of early endothelial cell genes, including VE-cadherin, Flk-1, and Tie2 at the mRNA and protein levels. ETV2 overexpression also induced the downregulation of a panel of smooth muscle cell and mesenchymal genes through epigenetic regulations, by decreasing the expression of DNA-modifying enzymes ten-eleven translocation dioxygenases. Adventitial Sca1+ cells grafted on the adventitial side of wire-injured femoral arteries increased vascular wall hyperplasia compared with control arteries with no grafted cells. Arteries seeded with ETV2-transduced cells, on the contrary, showed reduced hyperplasia compared with control.

Conclusions: These data give evidence that the genetic manipulation of vascular progenitors is a promising approach to improve vascular function after endothelial injury.

Keywords: adventitia; cell differentiation; stem cells; vascular diseases; vascular remodeling.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adventitia / metabolism*
  • Animals
  • Ataxin-1 / metabolism*
  • Biomarkers / metabolism
  • Cell Differentiation*
  • Cell Lineage*
  • Cells, Cultured
  • Disease Models, Animal
  • Endothelial Progenitor Cells / metabolism
  • Endothelial Progenitor Cells / transplantation*
  • Epigenesis, Genetic
  • Femoral Artery / metabolism
  • Femoral Artery / pathology
  • Femoral Artery / surgery*
  • Gene Expression Regulation
  • Genetic Therapy / methods*
  • Hyperplasia
  • Mice
  • Mice, Transgenic
  • Phenotype
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transduction, Genetic*
  • Vascular Remodeling*
  • Vascular System Injuries / genetics
  • Vascular System Injuries / metabolism
  • Vascular System Injuries / pathology
  • Vascular System Injuries / surgery*

Substances

  • Ataxin-1
  • Atxn1 protein, mouse
  • Biomarkers
  • Transcription Factors