MicroRNA-181a targets nanog in a subpopulation of CD34+ cells isolated from peripheral blood

Paul J. Mintz; Pål Sætrom; Vikash Reebye; Marie B. Lundbæk; Kaiqin Lao; John J. Rossi; Karin Ml Gaensler; Noriyuki Kasahara; Joanna P. Nicholls; Steen Jensen; Abdelali Haoudi; Mohamed M. Emara; Myrtle Ya Gordon; Nagy A. Habib

doi:10.1038/mtna.2012.29

MicroRNA-181a targets nanog in a subpopulation of CD34⁺ cells isolated from peripheral blood

Paul J. Mintz, Pål Sætrom, Vikash Reebye, Marie B. Lundbæk, Kaiqin Lao, John J. Rossi, Karin Ml Gaensler, Noriyuki Kasahara, Joanna P. Nicholls, Steen Jensen, Abdelali Haoudi, Mohamed M. Emara, Myrtle Ya Gordon, Nagy A. Habib

Research output: Contribution to journal › Article › peer-review

14 Scopus citations

Abstract

Exploiting the properties of stem cells by microRNA (miRNA) profiling offers an attractive approach to identify new regulators of stem cell fate. Although numerous miRNA have been screened from hematopoietic stem cells (HSC), the targets corresponding to many of these miRNA have not yet been fully elucidated. By miRNA profiling in a subpopulation of CD34+ cells isolated from peripheral blood, we have identified eight clusters of miRNA that were differentially expressed. Further analysis of one of the clusters by bioinformatics revealed that a miRNA, miR-181a, which is highly expressed in the adherent CD34+ cells, affects the expression levels of Nanog, a stem cell surrogate marker. We show specifically by reporter assay and mutational analysis that miR-181a tazgets a seedless 3' compensatory site in the 3'UTR of Nanog and affects gene expression. We demonstrate that inhibiting miR-181a upregulates the Nanog expression level, in addition to an increase in alkaline phosphatase activity. Our studies suggest that miR-181a may be important in controlling the expression level of Nanog in a subpopulation of CD34+ cells.

Original language	English (US)
Article number	e34
Pages (from-to)	e34
Journal	Molecular Therapy - Nucleic Acids
Volume	1
Issue number	8
DOIs	https://doi.org/10.1038/mtna.2012.29
State	Published - 2012
Externally published	Yes

Keywords

MiR-181a
Nanog
Stem cells

ASJC Scopus subject areas

Molecular Medicine
Drug Discovery

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Mintz, P. J., Sætrom, P., Reebye, V., Lundbæk, M. B., Lao, K., Rossi, J. J., Gaensler, K. M., Kasahara, N., Nicholls, J. P., Jensen, S., Haoudi, A., Emara, M. M., Gordon, M. Y., & Habib, N. A. (2012). MicroRNA-181a targets nanog in a subpopulation of CD34⁺ cells isolated from peripheral blood. Molecular Therapy - Nucleic Acids, 1(8), e34. [e34]. https://doi.org/10.1038/mtna.2012.29

MicroRNA-181a targets nanog in a subpopulation of CD34⁺ cells isolated from peripheral blood. / Mintz, Paul J.; Sætrom, Pål; Reebye, Vikash; Lundbæk, Marie B.; Lao, Kaiqin; Rossi, John J.; Gaensler, Karin Ml; Kasahara, Noriyuki; Nicholls, Joanna P.; Jensen, Steen; Haoudi, Abdelali; Emara, Mohamed M.; Gordon, Myrtle Ya; Habib, Nagy A.

In: Molecular Therapy - Nucleic Acids, Vol. 1, No. 8, e34, 2012, p. e34.

Research output: Contribution to journal › Article › peer-review

Mintz, Paul J. ; Sætrom, Pål ; Reebye, Vikash ; Lundbæk, Marie B. ; Lao, Kaiqin ; Rossi, John J. ; Gaensler, Karin Ml ; Kasahara, Noriyuki ; Nicholls, Joanna P. ; Jensen, Steen ; Haoudi, Abdelali ; Emara, Mohamed M. ; Gordon, Myrtle Ya ; Habib, Nagy A. / MicroRNA-181a targets nanog in a subpopulation of CD34⁺ cells isolated from peripheral blood. In: Molecular Therapy - Nucleic Acids. 2012 ; Vol. 1, No. 8. pp. e34.

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abstract = "Exploiting the properties of stem cells by microRNA (miRNA) profiling offers an attractive approach to identify new regulators of stem cell fate. Although numerous miRNA have been screened from hematopoietic stem cells (HSC), the targets corresponding to many of these miRNA have not yet been fully elucidated. By miRNA profiling in a subpopulation of CD34+ cells isolated from peripheral blood, we have identified eight clusters of miRNA that were differentially expressed. Further analysis of one of the clusters by bioinformatics revealed that a miRNA, miR-181a, which is highly expressed in the adherent CD34+ cells, affects the expression levels of Nanog, a stem cell surrogate marker. We show specifically by reporter assay and mutational analysis that miR-181a tazgets a seedless 3' compensatory site in the 3'UTR of Nanog and affects gene expression. We demonstrate that inhibiting miR-181a upregulates the Nanog expression level, in addition to an increase in alkaline phosphatase activity. Our studies suggest that miR-181a may be important in controlling the expression level of Nanog in a subpopulation of CD34+ cells.",

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