ArticleMolecular biology reports2013
miR-146a and miR-150 promote the differentiation of CD133+ cells into T-lymphoid lineage.
Article in Molecular biology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular mechanisms and clinical implications of miRNAs in drug resistance of colorectal cancer.Therapeutic advances in medical oncology · 2020Review
- Current Options and Future Directions in Immune Therapy for Glioblastoma.Frontiers in oncology · 2018Review
- MiR-146b protects cardiomyocytes injury in myocardial ischemia/reperfusion by targeting Smad4.American journal of translational research · 2017Article
- Magnet-Bead Based MicroRNA Delivery System to Modify CD133Stem cells international · 2016Article
- Detecting key genes regulated by miRNAs in dysfunctional crosstalk pathway of myasthenia gravis.BioMed research international · 2015Article
- Involvement of MicroRNA in T-Cell Differentiation and Malignancy.International journal of hematology-oncology and stem cell research · 2015Review
- MiR-146b Mediates Endotoxin Tolerance in Human Phagocytes.Mediators of inflammation · 2015Article
- Mir-302 cluster exhibits tumor suppressor properties on human unrestricted somatic stem cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- MiR-25 promotes gastric cancer cells growth and motility by targeting RECK.Molecular and cellular biochemistry · 2014Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs control the genes involved in hematopoietic stem cell (HSCs) survival, proliferation and differentiation. The over-expression of miR-146 and miR-150 has been reported during differentiation of HSCs into T-lymphoid lineage. Therefore, in this study we evaluated the effect of their over-expression on CD133+ cells differentiation to T cells. miR-146a and miR-150 were separately and jointly transduced to human cord blood derived CD133+ cells (>97% purity). We used qRT-PCR to assess the expression of CD2, CD3ε, CD4, CD8, CD25, T cell receptor alpha (TCR-α) and Ikaros genes in differentiated cells 4 and 8 days after transduction of the miRNAs. Following the over-expression of miR-146a, significant up-regulation of CD2, CD4, CD25 and Ikaros genes were observed (P<0.01). On the other hand, over-expression of miR-150 caused an increase in the expression of Ikaros, CD4, CD25 and TCR-α. To evaluate the combinatorial effect of miR-146a and miR-150, transduction of both miRNAs was concurrently performed which led to increase in the expression of Ikaros, CD4 and CD3 genes. In conclusion, it seems that the effect of miR-150 and miR-146a on the promotion of T cell differentiation is time-dependant. Moreover, miRNAs could be used either as substitutes or complements of the conventional differentiation protocols for higher efficiency.
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