thalidomide is more efficient than sodium butyrate in enhancing gata-1 and eklf gene expression in erythroid progenitors derived from hscs with β-globin gene mutation

نویسندگان

mohammad ali jalali far health research institute, research center of thalassemia & hemoglobinopathy, ahvaz jundishapur university of medical sciences, ahvaz, iran

ali dehghani fard sarem cell research center-scrc, sarem women’s hospital, tehran, iran

saiedeh hajizamani diagnosticlaboratory sciences and technology research center, school of paramedical sciences, shiraz university of medical sciences, shiraz, iran

majid mossahebi-mohammadi department of hematology, faculty of medical sciences, tarbiat modares university, tehran, iran

چکیده

background: efficient induction of fetal hemoglobin (hbf) is considered as an effective therapeutic approach in beta thalassemia. hbf inducer agents can induce the expression of γ-globin gene and produce high levels of hbf via different epigenetic and molecular mechanisms. thalidomide and sodium butyrate are known as hbf inducer drugs. material and methods : cd133 + stem cells were isolated from umbilical cord blood of a newborn with minor β-thalassemia in order to evaluate the effects of these two drugs on the in vitro expression of gata-1 and eklf genes as erythroid transcription factors. cd133 + stem cells were expanded and differentiated into erythroid lineage, and then treated with thalidomide and sodium butyrate and finally analyzed by quantitative real-time pcr. statistical analysis was performed using student’s t-test by spss software. results : thalidomide and sodium butyrate increased gata-1 and eklf gene expression, compared to the non-treated control (p<0.05). conclusion : thalidomide was more efficient than sodium butyrate in augmenting expression of gata-1 and eklf genes. it seems that gata-1 and eklf have crucial roles in the efficient induction of hbf by thalidomide.

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Thalidomide is more efficient than sodium butyrate in enhancing GATA-1 and EKLF gene expression in erythroid progenitors derived from HSCs with β-globin gene mutation

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عنوان ژورنال:
international journal of hematology-oncology and stem cell research

جلد ۱۰، شماره ۱، صفحات ۳۷-۴۱

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