The effect of aspirin on endothelial progenitor cell biology: Preliminary investigation of novel properties

Lou, Junyang; Povsic, Thomas J.; Allen, Jason D.; Adams, Stacie D.; Myles, Shelley; Starr, Aijing Z; Ortel, Thomas L.; Becker, Richard C.

doi:10.1016/j.thromres.2009.11.017

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Volume 126, Issue 3 , Pages e175-e179, September 2010

The effect of aspirin on endothelial progenitor cell biology: Preliminary investigation of novel properties☆

Junyang Lou
- Department of Medicine, Division of Cardiology, Duke Clinical Research Institute, USA
- Contributed equally to the study and manuscript.
Thomas J. Povsic
- Department of Medicine, Division of Cardiology, Duke Clinical Research Institute, USA
- Contributed equally to the study and manuscript.
Jason D. Allen
- Department of Medicine, Division of Cardiology, Duke Clinical Research Institute, USA
Stacie D. Adams
- Duke University School of Medicine, USA
- Duke University Medical Center, USA
Shelley Myles
- Department of Medicine, Division of Cardiology, Duke Clinical Research Institute, USA
Aijing Z Starr
- Department of Medicine, Division of Cardiology, Duke Clinical Research Institute, USA
Thomas L. Ortel
- Department of Medicine, Division of Hematology, USA
Richard C. Becker
- Department of Medicine, Division of Cardiology, Duke Clinical Research Institute, USA
- Department of Medicine, Division of Hematology, USA
- Corresponding author. 2400 Pratt Street, Durham, NC 27705.

Received 30 September 2009; received in revised form 5 November 2009; accepted 18 November 2009. published online 26 July 2010.

Abstract

Atherosclerosis develops in an environment of endothelial injury and inflammation. Circulating endothelial progenitor cells (EPCs) are required for vascular repair and restoration of normal endothelial function. We tested the hypothesis that the nonselective cyclooxygenase (COX) inhibitor aspirin (ASA) exerts an effect on circulating EPCs.

Methods

As part of a larger study evaluating the effect of aspirin dose in primary and secondary prevention, subjects (n=32) were assigned randomly to either 81mg or 325mg aspirin daily for two months, and circulating mononuclear cells were enumerated at the beginning of the study and after 2months using fluorescent antibodies against CD34 and CD133 as well as based on aldehyde dehydrogenase (ALDH) activity. Brachial artery endothelial function via flow-mediated dilation (BAFMD) and light transmittance platelet aggregometry in response to physiologic agonists was also determined.

Results

Subjects taking aspirin at the time of study entry had a lower numbers of CD133+/34+ cells compared to those not previously exposed (0.01% vs. 0.05% of MNCs, P<0.03). After 2months, subjects randomized to 81 vs. 325mg of ASA had no significant differences in the median numbers of EPCs, although mean numbers trended lower in the high dose group. Patients on chronic ASA therapy continued to have lower numbers of EPCs. Similar effects were observed in CD34 and CD 133 single-positive cells, as well as ALDH^br cells. BAFMD did not differ nor change significantly over time between aspirin dose groups. All patients had decreased ex vivo platelet aggregation in response to arachidonic acid and ADP stimulation.

Conclusions

Our preliminary studies suggest that aspirin exerts a time-dependent effect on circulating EPCs. Short-term exposure to differing doses of ASA had indeterminate effects on EPCs levels, suggesting that time of ASA exposure may play a more important role than dose. Determining the responsible mechanism(s) and the overall clinical relevance of these findings will require further investigation.