Beschreibung:
<jats:title>Abstract</jats:title><jats:p><jats:italic>In vitro</jats:italic>, C‐reactive protein (CRP) impairs endothelial progenitor cell (EPC) function; however, the influence of CRP on EPCs <jats:italic>in vivo</jats:italic> 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.</jats:p>