Simple jQuery Dropdowns
Please use this identifier to cite or link to this item:
Title: Accelerated telomere shortening in β-thalassemia/HbE patients
Authors: Pornthip Chaichompoo
Kovit Pattanapanyasat
Pranee Winichagoon
Suthat Fucharoen
Saovaros Svasti
Mahidol University
Keywords: Biochemistry, Genetics and Molecular Biology;Medicine
Issue Date: 1-Aug-2015
Citation: Blood Cells, Molecules, and Diseases. Vol.55, No.2 (2015), 173-179
Abstract: © 2015 Elsevier Inc. β-Thalassemia/HbE disease is caused by a defective β-globin synthesis that leads to accumulation of excess unbound α-globins, and consequently oxidative stress, ineffective erythropoiesis and chronic anemia. Cell replication and oxidative stress are factors contributing to erosion of telomeres responsible for maintaining genomic stability and cell replication capability. In this study, the rate of telomere shortening in β-thalassemia/HbE patients was compared to the rate of telomere shortening in normal individuals. Telomere length was determined from peripheral blood mononuclear cells of 43 β-thalassemia/HbE patients and 22 normal controls using Flow-FISH analysis. The telomere length was shown to be age-dependent in normal group (rs=0.715, P=0.002), whereas severity-dependent telomere shortening was observed in the patients. The telomere length of patients who had severe clinical symptoms (10.07±2.15%) was shorter than that of patients who showed mild symptoms (15.59±2.27%), moderate symptoms (14.50±1.41%) and those in the normal group (14.75±3.11%, P<0.05). Additionally, reticulocyte count and oxidative stress were correlated with telomere length. This indicates that increased oxidative stress and markedly enhanced erythropoiesis in β-thalassemia/HbE patients leads to accelerated telomere erosion in clinically severe patients.
ISSN: 10960961
Appears in Collections:Scopus 2011-2015

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.