Early accelerated senescence of circulating endothelial progenitor cells in premature coronary artery disease patients in a developing country - a case control study
1 Department of Cardiac Biochemistry, All India Institute of Medical Sciences, New Delhi, India
2 Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India
3 Center for Chronic Disease Control and CARRS COE, Public Health Foundation of India, New Delhi, India
4 Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India
5 National Brain Research Center, Manesar, Haryana, India
6 Department of Biostatistics, All India Institute of Medical Sciences, New Delhi, India
7 Public Health Foundation of India, New Delhi, India
8 Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, USA
BMC Cardiovascular Disorders 2013, 13:104 doi:10.1186/1471-2261-13-104Published: 19 November 2013
The decreased number and senescence of circulating endothelial progenitor cells (EPCs) are considered markers of vascular senescence associated with aging, atherosclerosis, and coronary artery disease (CAD) in elderly. In this study, we explore the role of vascular senescence in premature CAD (PCAD) in a developing country by comparing the numerical status and senescence of circulating EPCs in PCAD patients to controls.
EPCs were measured by flow cytometry in 57 patients with angiographically documented CAD, and 57 controls without evidence of CAD, recruited from random patients ≤ 50 years of age at All India Institute of Medical Sciences. EPC senescence as determined by telomere length (EPC-TL) and telomerase activity (EPC-TA) was studied by real time polymerase chain reaction (q PCR) and PCR– ELISA respectively.
The number of EPCs (0.18% Vs. 0.039% of total WBCs, p < 0.0001), and EPC-TL (3.83 Vs. 5.10 kb/genome, p = 0.009) were markedly lower in PCAD patients compared to controls. These differences persisted after adjustment for age, sex, BMI, smoking and medications. EPC-TA was reduced in PCAD patients, but was statistically significant only after adjustment for confounding factors (1.81 Vs. 2.20 IU/cell, unadjusted p = 0.057, adjusted p = 0.044).
We observed an association between increased vascular cell senescence with PCAD in a sample of young patients from India. This suggests that early accelerated vascular cell senescence may play an important mechanistic role in CAD epidemic in developing countries like India where PCAD burden is markedly higher compared to developed countries.