Send to

Choose Destination
See comment in PubMed Commons below
Atherosclerosis. 2007 May;192(1):92-9. Epub 2006 Aug 1.

High-density lipoprotein cholesterol regulates endothelial progenitor cells by increasing eNOS and preventing apoptosis.

Author information

Department of Medicine, Division of Neurology, Endothelial Progenitor Cell Laboratory, 771 HMRC, University of Alberta, Edmonton, Alta. T6G 2S2, Canada.



Endothelial progenitor cells (EPCs) are implicated as an important marker of endothelial function and cardiovascular risk. In the present study, we examined whether high-density lipoprotein (HDL) cholesterol plays a role in the peripheral EPC levels and its underlying mechanisms in the HDL cholesterol-induced elevation of EPCs.


For the clinical study, vascular risk factors and blood markers were measured and EPC colony forming units were counted after 7 days of culture. For the in vitro study, after 7 days of culture, EPCs were incubated in the presence or absence of HDL for 24h followed by measurements of eNOS and pro-MMP-9 expression and caspase-3 activity.


EPC colony levels significantly correlated with HDL levels (P=0.017). HDL treatment significantly increased eNOS protein expression in EPCs (P<0.001) while it significantly decreased pro-MMP-9 levels at the concentration of 50 microg/mL (P=0.002). Homocysteine treatment significantly increased caspase-3 activity whereas HDL significantly decreased it as compared to the homocysteine-only treated group.


The data demonstrate that EPC colony levels are significantly lower in individuals with low HDL and that HDL increases eNOS and decreases pro-MMP-9 in EPCs. HDL also prevents EPC apoptosis through inhibition of caspase-3 activity suggesting a possible mechanism for its positive effects on circulating EPC numbers.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center