Open AccessInfluence of Elevated Levels of C‐Reactive Protein on Circulating Endothelial Progenitor Cell Function
Author(s) -
Fasing Kevin A.,
Nissan Benjamin J.,
Greiner Jared J.,
Stauffer Brian L.,
DeSouza Christopher A.
Publication year - 2014
Publication title -
clinical and translational science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.303
H-Index - 44
eISSN - 1752-8062
pISSN - 1752-8054
DOI - 10.1111/cts.12137
Subject(s) - endothelial progenitor cell , c reactive protein , progenitor cell , medicine , vascular endothelial growth factor , endocrinology , apoptosis , staurosporine , angiogenesis , endothelial dysfunction , in vivo , endothelial stem cell , chemistry , andrology , in vitro , immunology , biology , stem cell , vegf receptors , inflammation , biochemistry , signal transduction , microbiology and biotechnology , protein kinase c
In vitro , C‐reactive protein (CRP) impairs endothelial progenitor cell (EPC) function; however, the influence of CRP on EPCs in vivo is unclear. We determined whether EPC function is impaired in adults with elevated plasma CRP concentrations, independent of other risk factors. EPCs were harvested from 75 adults (43 males, 32 females): 25 with low CRP (<1.0 mg/L); 25 with moderate CRP (1.0–3.0 mg/L); and 25 with high CRP (>3.0 mg/L). The capacity of EPCs to form colonies (colony assay), migrate (Boyden chamber), release angiogenic growth factor (ELISA) and resist apoptosis (active caspase‐3) was determined. There were no significant differences between the CRP groups in EPC colony formation (CFU), migration (AU) or the ability to release vascular endothelial growth factor (VEGF; pg/mL): low (13 ± 3 CFU; 1255 ± 100 AU; 126 ± 24 pg/mL); moderate (11 ± 3 CFU; 1137 ± 85 AU; 97 ± 14 pg/mL); and high (13 ± 4 CFU; 1071 ± 80 AU; 119 ± 22 pg/mL) CRP. Staurosporine‐stimulated activation of caspase‐3 was also similar between the low (2.3 ± 0.2 ng/mL), moderate (2.1 ± 0.3 ng/mL), and high (2.2 ± 0.2 ng/mL) CRP groups. These results indicate that elevations in plasma CRP are not associated with impaired EPC function. EPC dysfunction may not play a role in CRP‐related cardiovascular risk.