P-02/CO-02 : Endothelial Nitric Oxide Synthase (eNOS) gene expression of Endothelial Progenitor Cell (EPC) in Premature Coronary Artery Disease (PCAD) patients in Indian Population: A determinant of circulatory

posted Jan 26, 2017, 8:41 AM by sourav ghosh

Atanu Sen1Kranthi Vemparala1Ambuj Roy2Vinay Kumar Bahl2Dorairaj Prabhakaran3, Neera Nath4Subrata Sinha5Pradipta Nandi2Ravindra Mohan Pandey6Kolli Srinath Reddy7Ajay Manhapra8Ramakrishnan Lakshmy1
(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) Centre 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 Centre, 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


Introduction: A significant number of Ex-vivo and animal studies has already established that the reduced eNOS gene expression in EPC may leads to impaired mobilization of cells from bone marrow and that in turn results a reduced number of circulatory EPC in CAD patients. However in vivo eNOS gene expression of EPC from PCAD patients is yet to be known. Since in developing countries like India, the occurrence of cardiovascular disease at young age is markedly increasing, our present study aimed to investigate in vivo eNOS gene expression of EPC in PCAD patients and age matched healthy controls.
Method: Endothelial progenitor cells were isolated from peripheral blood on the basis of cell surface antigens CD34+/KDR+ by Magnetic Activated Cell sorting (MACS) method from 50 PCAD patients and 50 healthy controls. The intracellular eNOS gene expression was assessed by RT PCR method by using constitutive gene GAPDH as a reference gene. 
Result: A reduced eNOS gene expression (mean eNOS/GAPDH integrated density ratio)in EPC from PCAD patients compared to healthy controls were found (0.998±0.096/1.063±0.107) with a p-value of 0.002 and this difference was persisted even after adjustment for confounding factors like age, sex, BMI, smoking and statin therapy (p=0.002).
Conclusion: Our previous study had shown a significantly reduced number of CD34+/KDR+ cells in PCAD patients in comparison with healthy controls (.01868 ± .0176975/ .039972 ± .0299683; p<0.0001), which when supported by the result of the present study may delineate a possible cause of reduced circulatory level of EPC. Also as the study determined the eNOS gene expression directly in EPC isolated from study subjects, the result more realistically reflect the in vivo condition.

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