Publication: Effect of tumor necrosis factor-alpha on erythropoietinand erythropoietin receptor-induced erythroid progenitor cell proliferation in β-Thalassemia/Hemoglobin e patients
Issued Date
2015-01-01
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ISSN
13085263
13007777
13007777
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2-s2.0-84948763790
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Mahidol University
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SCOPUS
Bibliographic Citation
Turkish Journal of Hematology. Vol.32, No.4 (2015), 304-310
Suggested Citation
Dalina I. Tanyong, Prapaporn Panichob, Wasinee Kheansaard, Suthat Fucharoen Effect of tumor necrosis factor-alpha on erythropoietinand erythropoietin receptor-induced erythroid progenitor cell proliferation in β-Thalassemia/Hemoglobin e patients. Turkish Journal of Hematology. Vol.32, No.4 (2015), 304-310. doi:10.4274/tjh.2014.0079 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/36576
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Title
Effect of tumor necrosis factor-alpha on erythropoietinand erythropoietin receptor-induced erythroid progenitor cell proliferation in β-Thalassemia/Hemoglobin e patients
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Abstract
© 2015 Turkish Society of Hematology. All rights reserved. Objective: Thalassemia is one of the genetic diseases that cause anemia and ineffective erythropoiesis. Increased levels of several inflammatory cytokines have been reported in β-thalassemia and might contribute to ineffective erythropoiesis. However, the mechanism by which tumor necrosis factor-alpha (TNF-α) is involved in ineffective erythropoiesis in thalassemic patients remains unclear. The objective of this study is to investigate the effect of TNF-α on the erythropoietin (EPO) and erythropoietin receptor (EPOR) expression involved in proliferation of β-thalassemia/hemoglobin (Hb) E erythroid progenitor cells compared with cells from healthy subjects. Materials and Methods: CD34-positive cells were isolated from heparinized blood by using the EasySep® CD34 selection kit. Cells were then cultured with suitable culture medium in various concentrations of EPO for 14 days. The effect of TNF-α on percent cell viability was analyzed by trypan blue staining. In addition, the percentage of apoptosis and levels of EPOR protein were measured by flow cytometry. Results: Upon EPO treatment, a higher cell number was observed for erythroid progenitor cells from both healthy participants and β-thalassemia/Hb E patients. However, a reduction of apoptosis was found in EPO-treated cells especially for β-thalassemia/ Hb E patients. Interestingly, TNF-α caused higher levels of cell apoptosis and lower levels of EPOR protein in thalassemic erythroid progenitor cells. Conclusion: TNF-α caused a reduction in the level of EPOR protein and EPO-induced erythroid progenitor cell proliferation. It is possible that TNF-α could be involved in the mechanism of ineffective erythropoiesis in β-thalassemia/Hb E patients.