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Hits for promoting coronary endothelial angiogenic phenotype in n | 52072
Clinical & Experimental Cardiology

Clinical & Experimental Cardiology
Open Access

ISSN: 2155-9880

+44 1300 500008

Hits for promoting coronary endothelial angiogenic phenotype in normal rats


5th International Conference on Clinical & Experimental Cardiology

April 27-29, 2015 Philadelphia, USA

Anita A Mehta

Posters-Accepted Abstracts: J Clin Exp Cardiolog

Abstract :

Introduction: The VEGF induced angoiogenic phenotype of coronary endothelial cells is a key component for restoration of failing heart. However, there is no rectification of the factors that promote it. Objectives: To study effects of intermittent ischemia (I), telmisartan(T) and atorvastatin (A) alone and their combination on VEGF induced angiogenic responsiveness in coronary endothelial cells (VEGF-ang-res-cEC). Methods: Male wistar rats were divided into four groups, normal rats, T treated; A treated; and combination of T+A treated normal rats.Each group was further divided into two subgroups; sham heart and Iheart. Coronary endothelial cells (cEC) were isolated from each subgroup for study of ang-res-cEC and NO bioactivity. Results: I, T and A treated groups significantly increased VEGF-ang-res-cECas compared to their respective normal rats. The combination of any two of them and all showed significant increase in VEGF-ang-res-cEC as compared to alone treated groups. The effects of I, T,A, I+T, I+A, T+A and I+T+A were significantly inhibited by pre-treatment of cECs with eNOS inhibitor, NG-nitro-l-arginine methylester (l-NAME) and PI3K inhibitor, wortmannin whereas PKC inhibitor, chelerythrine, attenuated effects of all except T and T+A. Conclusion: Our data suggest that intermittent ischemia, telmisartan, atorvastatin, and their combination promotes the coronary angiogenic activity in normal rats via stimulating VEGF/PI3K+PKC/eNOS/NO pathway, and the order of improvement is I>T>A.

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