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CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

ABSTRACT: miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE65648 | GEO | 2015/06/30

SECONDARY ACCESSION(S): PRJNA274577

REPOSITORIES: GEO

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CodeLink™ Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with myeloproliferative disorder

Project description:miR-125a knockout mice develop myeloproliferave disorder (MPD). To investigate the molecular mechanisms of MPD induced by the loss of miR-125a, gene expression profiling on hematopoietic stem cells of miR-125a (+/+) and (+/-) MPD mice was performed using CodeLink Whole Genome DNA array analysis. Codelink Mouse Whole Genome Bioarrays were performed according to the manufacturer’s instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mice and miR-125a (+/-) heterozygous mice with MPD. One replicate per array.

2015-06-30 | E-GEOD-65648 | biostudies-arrayexpress

CodeLink Mouse Whole Genome Bioarray data from hematopoietic stem cells (HSCs) of miR-125a (+/+) wild-type and miR-125a knockout mice with myeloproliferative disorder (MPD)

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2015-12-31 | E-GEOD-69621 | biostudies-arrayexpress

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Expression data on Treg cells isolated from wildtype mice and miR-125a deficient mice

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Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector.

Project description:Hematopoietic stem/progenitor cell (HSPC) traits differ between genetically distinct mouse strains. For example, DBA/2 mice have a higher HSPC frequency compared to C57BL/6 mice. We performed a genetic screen for microRNAs that are differentially expressed between LSK, LS−K+, erythroid and myeloid cells isolated from C57BL/6 and DBA/2 mice. This analysis identified 131 microRNAs that were differentially expressed between cell types and 15 that were differentially expressed between mouse strains. Of special interest was an evolutionary conserved miR-cluster located on chromosome 17 consisting of miR-99b, let-7e and miR-125a. All cluster members were most highly expressed in LSKs and down-regulated upon differentiation. In addition, these microRNAs were higher expressed in DBA/2 cells compared to C57BL/6 cells, and thus correlated with HSPC frequency. To functionally characterize these microRNAs, we overexpressed the entire miR-cluster 99b/let-7e/125a and miR-125a alone in BM cells from C57BL/6 mice. Overexpression of the miR-cluster or miR-125a dramatically increased day-35 CAFC activity and caused severe hematopoietic phenotypes upon transplantation. We showed that a single member of the miR-cluster, namely miR-125a, is responsible for the majority of the observed miR-cluster overexpression effects. Finally, we performed genome-wide gene expression arrays and identified candidate target genes through which miR-125a may modulate HSPC fate.

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Project description:Umbilical cord blood (CB) is a non-invasive, convenient and broadly used source of hematopoietic stem cells (HSCs) for allogeneic stem cell transplantation. However, limiting numbers of HSCs remain a major constraint for its clinical application. One feasible option would be to expand HSCs to improve therapeutic outcome, however available protocols and the molecular mechanisms governing the self-renewal of HSC are unclear. Here we show that ectopic expression of a single miRNA, miR-125a, in purified murine and human multipotent progenitors (MPP) resulted in increased self-renewal and robust long-term multi-lineage repopulation in transplanted recipient mice. Using quantitative proteomics and Western blot analysis, we identified a restricted set of miR-125a targets which revealed the involvement of the MAP kinase signaling pathway in conferring long-term repopulating capacity to multipotent progenitors in human and mice. Our findings offer the innovative potential to use MPP with enhanced self-renewal activity to augment limited sources of HSC to improve clinical protocols.

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Expression data from bone marrow neutrophils with or without LPS stimulation in wild type and miR-125a deficient mice

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