ArticleHaematologica2010
Mechanism of human Hb switching: a possible role of the kit receptor/miR 221-222 complex.
Article in Haematologica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05806684 (Correlation Between Hyperbilirubinemia and Retinopathy of Prematurity in Preterm Infants of Very Low Birth Weight and Less Than 32 Weeks Gestational Age), which is not on this map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Correlation Between Hyperbilirubinemia and Retinopathy of Prematurity in Preterm Infants of Very Low Birth Weight and Less Than 32 Weeks Gestational Age: a Retrospective Study
Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Dysregulated Expression of miR-222 and miR-15a in Transfusion-Dependent Thalassemia: Associations with Torque Teno Virus and Cytomegalovirus Infections.International journal of hematology-oncology and stem cell research · 2025Article
- miRNA Expression Associated with HbF in Saudi Sickle Cell Anemia.Medicina (Kaunas, Lithuania) · 2022Article
- The Role of miRNAs as Therapeutic Tools in Sickle Cell Disease.Medicina (Kaunas, Lithuania) · 2021Review
- Erythrocyte microRNAs: a tiny magic bullet with great potential for sickle cell disease therapy.Annals of hematology · 2021Review
- miR-30a regulates γ-globin expression in erythoid precursors of intermedia thalassemia through targeting BCL11A.Molecular biology reports · 2020Article
- Construction and Analysis of a Long Non-Coding RNA (lncRNA)-Associated ceRNA Network in β-Thalassemia and Hereditary Persistence of Fetal Hemoglobin.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- MYC-related microRNAs signatures in non-Hodgkin B-cell lymphomas and their relationships with core cellular pathways.Oncotarget · 2018Article
- Fetal hemoglobin in sickle cell anemia: The Arab-Indian haplotype and new therapeutic agents.American journal of hematology · 2017Review
- Featured Article: Modulation of fetal hemoglobin in hereditary persistence of fetal hemoglobin deletion type-2, compared to Sicilian δβ-thalassemia, by BCL11A and SOX6-targeting microRNAs.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- A candidate transacting modulator of fetal hemoglobin gene expression in the Arab-Indian haplotype of sickle cell anemia.American journal of hematology · 2016Article
- Elevated levels of miR-210 correlate with anemia in β-thalassemia/HbE patients.International journal of hematology · 2016Article
- Advances in understanding erythropoiesis: evolving perspectives.British journal of haematology · 2016Review
- MicroRNA Expression in β-Thalassemia and Sickle Cell Disease: A Role in The Induction of Fetal Hemoglobin.Cell journal · 2016Review
- MiR-218 Inhibits Erythroid Differentiation and Alters Iron Metabolism by Targeting ALAS2 in K562 Cells.International journal of molecular sciences · 2015Article
- Article
- A feedback loop consisting of microRNA 23a/27a and the β-like globin suppressors KLF3 and SP1 regulates globin gene expression.Molecular and cellular biology · 2013Article
- Emodin can induce K562 cells to erythroid differentiation and improve the expression of globin genes.Molecular and cellular biochemistry · 2013Article
- MicroRNA-486-3p regulates γ-globin expression in human erythroid cells by directly modulating BCL11A.PloS one · 2013Article
- Fetal haemopoiesis marking low-grade urinary bladder cancer.British journal of cancer · 2012Article
- MicroRNAs: Allies or foes in erythropoiesis?Journal of cellular physiology · 2012Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe human hemoglobin switch (HbF-->HbA) takes place in the peri/post-natal period. In adult life, however, the residual HbF (<1%) may be partially reactivated by chemical inducers and/or cytokines such as the kit ligand (KL). MicroRNAs (miRs) play a pivotal role in normal hematopoiesis: downmodulation of miR-221/222 stimulates human erythropoietic proliferation through upmodulation of the kit receptor. DESIGN AND
methodsWe have explored the possible role of kit/KL in perinatal Hb switching by evaluating: i) the expression levels of both kit and kit ligand on CD34(+) cells and in plasma isolated from pre-, mid- and full-term cord blood samples; ii) the reactivation of HbF synthesis in KL-treated unilineage erythroid cell cultures; iii) the functional role of miR-221/222 in HbF production.
resultsIn perinatal life, kit expression showed a gradual decline directly correlated to the decrease of HbF (from 80-90% to <30%). Moreover, in full-term cord blood erythroid cultures, kit ligand induced a marked increase of HbF (up to 80%) specifically abrogated by addition of the kit inhibitor imatinib, thus reversing the Hb switch. MiR-221/222 expression exhibited rising levels during peri/post-natal development. In functional studies, overexpression of these miRs in cord blood progenitors caused a remarkable decrease in kit expression, erythroblast proliferation and HbF content, whereas their suppression induced opposite effects.
conclusionsOur studies indicate that human perinatal Hb switching is under control of the kit receptor/miR 221-222 complex. We do not exclude, however, that other mechanisms (i.e. glucocorticoids and the HbF inhibitor BCL11A) may also contribute to the peri/post-natal Hb switch.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.