این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
International Journal of Hematology-Oncology and Stem Cell Research، جلد ۶، شماره ۱، صفحات ۱۱-۱۲
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Epigenetic modulations on the fetal hemoglobin induction
چکیده انگلیسی مقاله In recent years of experience fetal hemoglobin (HbF) induction considers as novel therapeutic approach for β-thalassemia and sickle cell in therapeutic approaches. Several pharmacologic agents such as Hydroxyurea, Azacytidine, butyrate deriviates and immunomodulator drugs like Pomalidomide and Lnalidomide could able to up-regulate HbF level with different molecular and epigenetic paterns (1-4). The epigenetic modifications including DNA methylation and histon modification play an important role in γ-globin gene over-expression in mature stage of erythropoiesis. Butyrate and Azacytidine consider as well-known histon deacetylase (HDAC) inhibitor and DNA methyltransferase-1 (DNMT-1) inhibitor. These agents reversed the switching of β-globin gene to γ-globin gene with decreasing of DNA methylation in CpG islands of β-like globin genes promoter. Also, these two agents increase histon H3 and H4 acetylation at the promoter of β-globin cluster. These epigenetic changes result in the efficient up-regulation of γ-globi gene at different developmental stages of erythropoiesis (5,6). Thalidomide could able to increase H4 acetylation via activation of p38 in MAPK pathway for its HbF induction (7). Other studies show the potential role of Pomalidomide in γ-globin gene induction with increasing of acetylation of histon H3 lysines 9 and 14 (H3K9 & H3K14) at the promoters of human β-globin genes (8). Recently, we studied the invitro effects of single and combination treatments of Thalidomide and Sodium butyrate on the methylation of histon H3K27 as heterochromatin mark at the promoter of β-globin cluster. We showed that Thalidomide much effective in suppresseion of H3K27 methylation in comparison with Sodium butyrate. Besides, Thalidomide has more potential to decrease H3K27 methylation than combination treatment of Thalidomide and Sodium butyrate, regarding to the synergistic effect of combination treatment on γ-globin gene induction compared to single treatments (9-11). These data suggests that combination treatment of Thalidom and Sodium butyrate could play critical role on γ-globin gene induction with different epigenetic models. In conclusion, we suggests further investigation on epigenetic mechanisms of γ-globin gene induction for elucidation the molecular mechanisms of gene induction.
کلیدواژه‌های انگلیسی مقاله #No Keywords#
نویسندگان مقاله سعید کاویانی | saeid kaviani
department of hematology and blood banking, faculty of medical sciences, tarbiat modares university,tehran, iran

سازمان اصلی تایید شده: دانشگاه تربیت مدرس (Tarbiat modares university)

مهرداد نوروزی نیا | mehrdad noruzinia
department of medical genetic, faculty of medical sciences, tarbiat modares university, tehran, iran

سازمان اصلی تایید شده: دانشگاه تربیت مدرس (Tarbiat modares university)

نجم الدین ساکی | najmaldin saki
thalassemia and hemoglobinopathy research center, jundishapur university of medical sciences, ahvaz, iran


اسماعیل مرتاض | esmaeil mortaz
division of pharmacology, utrecht institute for pharmaceutical sciences, utrecht university, the netherlands
نشانی اینترنتی http://ijhoscr.tums.ac.ir/index.php/ijhoscr/article/view/321
فایل مقاله فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Articles
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات