ApoA-I induced CD31 in bone marrow-derived vascular progenitor cells increases adhesion: Implications for vascular repair

Academic Article


  • Transgenic over expression of apolipoprotein A-I (ApoA-I) the major structural apolipoprotein of HDL appears to convey the most consistent and strongest anti atherogenic effect observed in animal models so far. We tested the hypothesis that ApoA-I mediates its cardio protective effects additionally through ApoA-I induced differentiation of bone marrow-derived progenitor cells in vitro. This study demonstrates that lineage negative bone marrow cells (lin- BMCs) alter and differentiate in response to free ApoA-I. We find that lin- BMCs in culture treated with recombinant free ApoA-I at a concentration of 0.4 μM are twice as large in size and have altered cell morphology compared to untreated cells; untreated cells retain the original spheroid morphology. Further, the total number of CD31 positive cells in the ApoA-I treated population consistently increased by two fold. This phenotype was significantly reduced in untreated cells and points towards a novel ApoA-I dependent differentiation. A protein lacking its best lipid-binding region (ApoA-IΔ10) did not stimulate any changes in the lin-BMCs indicating that ApoA-I may mediate its effects by regulating cholesterol efflux. The increased CD31 correlates with an increased ability of the lin- BMCs to adhere to both fibronectin and mouse brain endothelial cells. Our results provide the first evidence that exogenous free ApoA-I has the capacity to change the characteristics of progenitor cell populations and suggests a novel mechanism by which HDL may mediate its cardiovascular benefits.
  • Digital Object Identifier (doi)

    Author List

  • Mythreye K; Satterwhite LL; Davidson WS; Goldschmidt-Clermont PJ
  • Start Page

  • 703
  • End Page

  • 709
  • Volume

  • 1781
  • Issue

  • 11-12