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Gene Regulation and Systems Biology

Endothelial Nitric Oxide Synthase (–786T>C) and Endothelin-1 (5665G.T) Gene Polymorphisms as Vascular Dysfunction Risk Factors in Sickle Cell Anemia

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Gene Regulation and Systems Biology 2016:10 67-72

Original Research

Published on 28 Jul 2016

DOI: 10.4137/GRSB.S38276


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Abstract

Sickle cell anemia (SCA) patients have vascular complications, and polymorphisms in endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) genes were associated with ET-1 and nitric oxide disturbance. We investigate the association of ET-1 5665G.T and eNOS –786T>C polymorphisms with soluble adhesion molecules (sVCAM-1 and sICAM-1), biochemical markers, and medical history. We studied 101 SCA patients; carriers of eNOS minor allele (C) had the highest levels of sVCAM-1, and carriers of ET-1 minor allele had more occurrence of acute chest syndrome (ACS). The multivariate analysis suggested the influence of the ET-1 gene on ACS outcome and an association of the eNOS gene with upper respiratory tract infection. We suggest that eNOS and ET-1 gene polymorphisms can influence SCA pathophysiology and that eNOS variant in SCA patients might be important to nitric oxide activity and vascular alteration. We found an association of the ET-1 minor allele in ACS, showing the importance of genetic screening in SCA.



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