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

Journal 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 microM 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-I Delta 10) 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.

Full Text

Duke Authors

Cited Authors

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

Published Date

  • November 2008

Published In

Volume / Issue

  • 1781 / 11-12

Start / End Page

  • 703 - 709

PubMed ID

  • 18775511

International Standard Serial Number (ISSN)

  • 0006-3002

Digital Object Identifier (DOI)

  • 10.1016/j.bbalip.2008.08.002

Language

  • eng

Conference Location

  • Netherlands