Evidence map›Paper›PMID 32406020›Full record

ArticleMolecular biology reports2020

miR-30a regulates γ-globin expression in erythoid precursors of intermedia thalassemia through targeting BCL11A.

Mohammad Ali Gholampour, Marjan Asadi, Mehran Naderi, Azita Azarkeivan, Masoud Soleimani, Amir Atashi

Abstract read
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In one paragraph

Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Transcriptional Repressor BCL11A in Erythroid Cells.Advances in experimental medicine and biology · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Mohammad Ali GholampourDepartment of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Marjan AsadiHematology Department, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mehran NaderiDepartment of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Azita AzarkeivanPediatric Hematology-Oncology, Iranian Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Thalassemia Clinic, Tehran, Iran.
Masoud SoleimaniDepartment of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Amir AtashiStem Cell and Tissue Engineering Research Center, Shahroud University of Medical Sciences, Shahroud, Iran. atashia@shmu.ac.ir.ORCID http://orcid.org/0000-0002-3889-5642
Tarbiat Modares University · IRHigh Institute for Education and Research in Transfusion Medicine · IRShahroud University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

Tarbiat Modares University 9620822001
6 · The paper itself

Abstract

Patients with β-thalassemia suffer from a lack or absence of the beta-globin chain of normal hemoglobin (Hb). Therefore, an increase in fetal Hb (HbF) levels could improve the clinical status of these patients. Downregulation of BCL11A, a key regulatory transcription factor, could ameliorate the clinical status of thalassemic patients by increasing HbF levels. miR-30a expression and its relationship with the BCL11A gene in erythroid precursors was explored in patients with β-thalassemia. The relevance of miR-30a to clinical parameters was also investigated. We evaluated the expressions of miR-30a, BCL11A, and γ-globin genes by quantitative real-time PCR (qRT-PCR) on isolated erythroid precursors from peripheral blood samples of β-thalassemia intermedia (TI) patients and in bone marrow samples from healthy individuals as controls. The correlation between miR-30a expression and clinical indices that included HbF levels, ferritin, and the frequency of blood transfusions were assessed. We observed increased expression of miR-30a in conjunction with decreased BCL11A expression and elevated γ-globin and HbF levels. Patients with elevated miR-30a expression had a higher percentage of HbF and a lower level of ferritin. In addition, we observed that overexpression of miR-30a in erythroid precursor cells led to reduced BCL11A expression and was associated with elevated γ-globin expression. Our findings showed the importance of miR-30a in BCL11A and HbF regulation, and in the clinical status of patients with β-thalassemia.

Indexed as

Adultbeta-Globinsbeta-ThalassemiaErythroid Precursor CellsFemaleFetal Hemoglobingamma-GlobinsGene Expression RegulationHumansMaleMicroRNAsRepressor ProteinsTranscription FactorsBCL11A protein, humanbeta-GlobinsFetal Hemoglobingamma-GlobinsMicroRNAsMIRN30b microRNA, humanRepressor ProteinsTranscription FactorsBCL11AHbFmiR-30aβ-thalassemia

Identifiers

PMID32406020
OpenAlexW3025563510

What OpenQuestion holds

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Registered trials

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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.