Abstract 5458: Telomere Length is Reduced in Endothelial Progenitor Cells (EPCs) from Subjects with Prehypertension and Hypertension and Relates to Impaired Epc In Vivo Re-Endothelialisation Capacity
Endothelial progenitor cells promote endothelial repair. Telomere shortening has been shown to be associated with cell turnover. We therefore examined telomerase activity and telomere length of EPCs from prehypertensive and hypertensive subjects, and determined the relation to EPC in vivo function. EPCs were isolated from hypertensive (n=20), prehypertensive (n=16) and healthy subjects (HS; n=16) without other cardiovascular risk factors. EPC telomerase activity was determined by an ELISA assay kit, telomere length by real time PCR analysis. EPC senescence was measured by senescence-associated beta-galactosidase staining (SA-β-Gal). EPC in vivo re-endothelialisation capacity was examined by injection of EPCs (5x10^5) into nude mice with carotid injury. Re-endothelialised area was determined after three days. EPC telomerase activity was reduced, SA-β-Gal activity was increased in prehypertension and hypertension. Furthermore, EPC telomere length was decreased in hypertensive and prehypertensive subjects as compared to HS (7±1 vs. 9±1 vs. 12±2 kb, p<0.05). Reduced telomere length was related to impaired EPC in vivo re-endothelialisation capacity (r=0.32, p<0.05), and was inversely related to systolic blood pressure (see figure⇓). The present study demonstrates for the first time that telomerase activity and telomere length are reduced in EPCs of prehypertensive and hypertensive subjects and are related to impaired EPC in vivo function and the degree of hypertension. These findings suggest that EPC senescence is an early event in the development of hypertension and may contribute to progression of vascular disease.