alexa Mechanisms Underlying The Development Of Pulmonary Arterial Hypertension In Secretin Gene Deficiency
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Joint Conference on 17th European Heart Disease and Heart Failure Congress and 2nd International Conference on Cardiovascular Medicine and Cardiac Surgery
March 15-17, 2017 London, UK

Revathi Sekar
University of Hong Kong, Hong Kong
Posters & Accepted Abstracts: J Clin Exp Cardiolog
DOI: 10.4172/2155-9880.C1.066
Abstract
Idiopathic (primary) pulmonary arterial hypertension (IPAH) is a disease with fatal prognosis, as seen by progressive right heart failure within three years after diagnosis. Extensive research in recent past has led to substantial advancement in our understanding of the genetic basis and pathophysiology of PAH resulting in better and more effective treatment strategies. However, very little is known about the pathological mechanisms underlying PAH and being a complex multi-factorial disease. Secretin (SCT), a braingut peptide hormone, has been found in the past to have pleiotropic functions including its important role in water homeostasis. We have found pathological features of PAH after targeted deletion of SCT gene and have explored the mechanisms underlying. Histopathological examinations and immunohistochemical staining of CD31 (endothelial cell specific marker protein) revealed development of pathological features of PAH in lungs of SCT knockout (SCT-/-) when compared to C57 mice such as thickened arterial wall, enlarged medial area and narrowed lumen. TUNEL staining and immuno fluorescent co-localization studies with CD31 revealed increased endothelial cell (EC) apoptosis in pulmonary arteries of SCT-/- mice. This is likely to be triggered by low levels of lung-vascular endothelial growth factor (VEGF) -transcripts measured by real-time PCR and -protein measured in bronchio alveolar fluid. Deletion of SCT gene leads to spontaneous development of moderate PAH in mice. It might be initiated by EC apoptosis in pulmonary arteries, possibly due to reduced VEGF levels, resulting in increased pulmonary pressure and pulmonary vascular remodeling. Although not an exact reflection of human idiopathic PAH, SCT-/- mice would be useful for obtaining mechanistic and therapeutic insights underlying PAH.
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