A sustained and pancellular reversal of gamma-globin gene silencing in adult human erythroid precursor cells.
نویسندگان
چکیده
We systematically compared cytokine-mediated increases or decreases in proliferation with globin gene and protein expression in adult human erythroblasts. Despite their opposite effects on growth, stem cell factor (SCF) and transforming growth factor beta (TGF-B) had synergistic effects with respect to fetal hemoglobin (HbF): average HbF/HbF + adult hemoglobin (HbA) ratio in erythropoietin (EPO) = 1.4 +/- 1.0%; EPO + TGF-B = 10.8 +/- 1.9%; EPO + SCF = 19.1 +/- 6.2%; and EPO + SCF + TGF-B (EST) = 39.3 +/- 6.3%. Polymerase chain reaction (PCR) revealed significant increases in gamma-globin transcripts that were balanced by reduced beta-globin transcripts. Single-cell quantitative PCR demonstrated a complete reversal of gamma-globin gene silencing with detectable gamma-globin mRNA in more than 95% of the cells. Immunostaining with HbF antibodies also showed a pancellular distribution in EST (96.2 +/- 0.01% HbF positive) compared with a heterocellular distribution in EPO (42.9 +/- 0.01% HbF positive). As shown here for the first time, a robust and pancellular reversal of gamma-globin gene silencing among hemoglobinized erythroblasts from adult humans may be achieved in the absence of hereditary mutation or direct genomic manipulation.
منابع مشابه
RED CELLS A sustained and pancellular reversal of gamma-globin gene silencing in adult human erythroid precursor cells
We systematically compared cytokinemediated increasesordecreases inproliferation with globin gene and protein expression in adult human erythroblasts. Despite their opposite effects on growth, stem cell factor (SCF) and transforming growth factorbeta (TGF-B) had synergistic effects with respect to fetal hemoglobin (HbF): average HbF/HbF adult hemoglobin (HbA) ratio in erythropoietin (EPO) 1.4 1...
متن کاملIGF2BP1 overexpression causes fetal-like hemoglobin expression patterns in cultured human adult erythroblasts.
Here we investigated in primary human erythroid tissues a downstream element of the heterochronic let-7 miRNA pathway, the insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), for its potential to affect the hemoglobin profiles in human erythroblasts. Comparison of adult bone marrow to fetal liver lysates demonstrated developmental silencing in IGF2BP1. Erythroid-specific overexpressi...
متن کاملIdentification of a PRMT5-dependent repressor complex linked to silencing of human fetal globin gene expression.
Defining the molecular mechanisms underpinning fetal (gamma) globin gene silencing may provide strategies for reactivation of gamma-gene expression, a major therapeutic objective in patients with beta-thalassemia and sickle cell disease (SCD). We have previously demonstrated that symmetric methylation of histone H4 Arginine 3 (H4R3me2s) by the protein arginine methyltransferase PRMT5 is require...
متن کاملبررسی بیان ژن های موثر در سنتز گاما گلوبین قبل و بعد از تمایز سلول های بنیادی خونساز به رده سلول های اریتروئیدی
Background and aim: Induction of fetal hemoglobin (Hb-F) can improve the patients’ symptoms of haemoglobinopathies. Several factors can induce gamma globin gene expression and increased Hb-F levels in patients. In this study, the expression of genes is involved in regulation of gamma globin synthesis such as PIPKII-alpha BCL11a, and miR-30a during CD34+ hematopoietic stem cell differentiation i...
متن کاملFetal hemoglobin silencing in humans.
Interruption of the normal fetal-to-adult transition of hemoglobin expression should largely ameliorate sickle cell and beta-thalassemia syndromes. Achievement of this clinical goal requires a robust understanding of gamma-globin gene and protein silencing during human development. For this purpose, age-related changes in globin phenotypes of circulating human erythroid cells were examined from...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Blood
دوره 105 1 شماره
صفحات -
تاریخ انتشار 2005