Role of bone marrow-derived cells in the genetic control of restenosis

Arterioscler Thromb Vasc Biol. 2009 Oct;29(10):1551-7. doi: 10.1161/ATVBAHA.109.188326. Epub 2009 Jul 30.


Objective: Angiographic indexes of restenosis after coronary stent placement in patients show a bimodal pattern suggesting the existence of two populations with different risk of restenosis. This is reflected in the arterial remodeling response of inbred mouse strains arguing for a genetic control of the mechanisms leading to lumen narrowing. As bone marrow-derived cells (BMCs) contribute to vascular healing after arterial injury, we investigated the role of BMCs in the genetic control of restenosis.

Methods and results: 129X1/SvJ mice developed significantly more neointima and late lumen loss compared to C57BL/6 mice. Gene expression analysis of intimal tissue revealed major differences in the expression of inflammatory and hematopoietic stem and progenitor cell-associated genes in response to arterial injury. In 129X1/SvJ mice stronger mobilization of lin(-)sca-1(+)CXCR4(+) cells was observed after vascular injury. Bone marrow transplantation identified the extent of neointima formation as clearly dependent on the genetic background of BMCs (ie, mice with 129X1/SvJ BMCs developed more intimal hyperplasia). The inflammatory response and the recruitment of BMCs to the site of arterial injury were significantly increased in mice with 129X1/SvJ BMCs.

Conclusions: The genetically controlled mechanisms leading to lumen narrowing in vascular remodeling are dependent on mobilization and recruitment capacities of particular BMCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Ly / physiology
  • Bone Marrow Cells / physiology*
  • Bone Marrow Transplantation
  • Cell Movement
  • Endothelial Cells / physiology
  • Femoral Artery / pathology*
  • Gene Expression Profiling
  • Hyperplasia
  • Male
  • Membrane Proteins / physiology
  • Mice
  • Mice, Inbred C57BL
  • Receptors, CXCR4 / genetics
  • Species Specificity
  • Tunica Intima / pathology
  • Vascular Diseases / genetics*


  • Antigens, Ly
  • CXCR4 protein, mouse
  • Ly6a protein, mouse
  • Membrane Proteins
  • Receptors, CXCR4