Bone mesenchymal stem cells contributed to the neointimal formation after arterial injury

PLoS One. 2013 Dec 9;8(12):e82743. doi: 10.1371/journal.pone.0082743. eCollection 2013.

Abstract

Objectives: Recent findings suggest that in response to repair-to-injury bone marrow mesenchymal stem cells (BMSCs) participate in the process of angiogenesis. It is unclear what role BMSCs play in the structure of the vessel wall. In present study, we aimed to determine whether BMSCs had the capacity of endothelial cells (ECs).

Methods: BMSCs were separated and cultured. FACS and RT-PCR analysis confirmed the gene expression phenotype. The capacity of migration and adhesion and the ultrastructure of BMSCs were examined. The effect of BMSCs transplantation on the vascular repair was investigated in a murine carotid artery-injured model.

Results: BMSCs could express some markers and form the tube-like structure. The migration and adhesion capacity of BMSCs increased significantly after stimulated. In addition, BMSCs had the intact cell junction. In vivo the local transfer of BMSCs differentiated into neo-endothelial cells in the injury model for carotid artery and contributed to the vascular remodeling.

Conclusion: These results showed that BMSCs could contribute to neointimal formation for vascular lesion and might be associated with the differentiation into ECs, which indicated the important therapeutic implications for vascular diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arteries / injuries*
  • Arteries / metabolism*
  • Biomarkers
  • Cell Adhesion / genetics
  • Cell Differentiation
  • Cell Movement / genetics
  • Endothelial Cells / cytology
  • Endothelial Cells / metabolism
  • Female
  • Gene Expression
  • Immunophenotyping
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Mesenchymal Stem Cell Transplantation
  • Mesenchymal Stem Cells / cytology
  • Mesenchymal Stem Cells / metabolism*
  • Mice
  • Neointima / metabolism*
  • Neovascularization, Physiologic / physiology
  • Phenotype
  • RNA, Messenger / genetics
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism
  • Vascular System Injuries / genetics
  • Vascular System Injuries / metabolism*

Substances

  • Biomarkers
  • RNA, Messenger
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1

Grants and funding

This work was supported by the grant from the National Natural Science Foundation of China (no. 81270355) and the grants from the Fund of Hubei Province Educational Department (Q20122805) and the Fund of Hubei University of Science and Technology (BK1002, ZX1125, and PY1107). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.