Regulation of vasculogenesis by platelet-mediated recruitment of bone marrow-derived cells. Review uri icon

Overview

MeSH

  • Bone Marrow Cells
  • Chemokine CXCL12
  • Endothelial Cells
  • Humans
  • Thrombospondins
  • Vascular Endothelial Growth Factor A

MeSH Major

  • Blood Platelets
  • Cell Differentiation
  • Neovascularization, Physiologic

abstract

  • Bone marrow-derived cells contribute to physiological and pathological vascular remodeling throughout ontogenesis and adult life. During tissue regeneration and tumor growth, the release of cytokines and chemokines mediates the recruitment of hematopoietic and endothelial progenitor cells that contribute to the assembly of neovessels. Current evidence implies that platelets contribute structurally and instructively to vascular remodeling. Platelets adhere almost immediately to exposed or activated endothelium, and they are major storage and delivery vehicles for pro- and antiangiogenic growth factors including VEGF-A and thrombospondin (TSP), and cytokines and chemokines, such as stromal-derived factor 1 (SDF-1). By site-specific deployment of these factors, platelets orchestrate the local angiogenic stimulus within a tissue and direct the recruitment and differentiation of circulating bone marrow-derived cells. These insights have profound clinical implications; inhibition of platelet-deployed growth factors or their receptors may be an effective strategy to block tumor growth, whereas activation of these pathways may be used to accelerate revascularization and tissue regeneration.

publication date

  • February 2008

has subject area

  • Blood Platelets
  • Bone Marrow Cells
  • Cell Differentiation
  • Chemokine CXCL12
  • Endothelial Cells
  • Humans
  • Neovascularization, Physiologic
  • Thrombospondins
  • Vascular Endothelial Growth Factor A

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1161/ATVBAHA.107.151159

PubMed ID

  • 18096826

Additional Document Info

start page

  • 217

end page

  • 222

volume

  • 28

number

  • 2