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Differential mRNA expression upon microRNA-125a overexpression in murine hematopoietic cells

ABSTRACT: Differential mRNA expression upon microRNA-125a overexpression in murine hematopoietic cells

PROVIDER: PRJNA664058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12659900_1.fastq.gz	Fastqsanger.gz
	SRR12659900_2.fastq.gz	Fastqsanger.gz
	SRR12659901_1.fastq.gz	Fastqsanger.gz
	SRR12659901_2.fastq.gz	Fastqsanger.gz
	SRR12659902_1.fastq.gz	Fastqsanger.gz

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Differential mRNA expression upon microRNA-125a overexpression in murine hematopoietic cells

Project description:We report differential gene expression in hematopoietic cells (lineage-Sca+) upon overexpression and transplantation of murine hematopoietic stem cells.

2021-02-11 | GSE158126 | GEO

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.

2011-12-15 | GSE33689 | GEO

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

2011-12-15 | E-GEOD-33689 | biostudies-arrayexpress

MicroRNA-125a-5p overexpression in human macrophages

Project description:MicroRNA-125a-5p overexpression in human macrophages

| PRJNA414033 | ENA

Genetic Screen Identifies MicroRNA Cluster 99b/let-7e/125a as a Regulator of Primitive Hematopoietic Cells

Project description:This SuperSeries is composed of the following subset Series: GSE33689: Expression profiles of HSPCs overexpressing microRNA cluster 99b/let-7e/125a, miR-125a, miR-155 and empty vector. GSE33690: MicroRNA profiles of four developmentally related hematopoietic cell types isolated from the BM of B6 and D2 mice. Refer to individual Series

2011-12-15 | E-GEOD-33691 | 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)

Project description:miR-125a knockout mice develop myeloproliferative 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 (+/+), (+/-) MPD, and (-/-) MPD mice was performed by using CodeLinkTM Whole Genome DNA array analysis. CodeLink Mouse Whole Genome Bioarrays were performed according to the manufacturerâs instruction on total RNA extracted from hematopoietic stem cells of miR-125a (+/+) wild-type mouse, miR-125a (+/-) heterozygous mouse with MPD, and miR-125a (-/-) homozygous mouse with MPD. One replicate per array.

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MicroRNA-125a-5p overexpression in human macrophages

Project description:Systemic juvenile idiopathic arthritis (SJIA) is a severe childhood arthropathy with features of autoinflammation. Monocytes and macrophages in SJIA have a complex phenotype with both pro- and anti-inflammatory properties that combine features of several well characterized in vitro conditions used to activate macrophages. An important anti-inflammatory phenotype is expression of CD163, a scavenger receptor that sequesters toxic pro-inflammatory complexes that is highly expressed in both active SJIA and macrophage activation syndrome (MAS). CD163 is most strongly upregulated by IL-10 (M(IL-10)), and not by other conditions that reflect features seen in SJIA monocytes such as M(LPS+IC). MicroRNA play key roles balancing and integrating cellular signals such as those in macrophage polarization, and as such we hypothesize microRNA regulate macrophage functional responses in SJIA including CD163 expression in vitro. We find that two microRNA previously found to be elevated in active SJIA, miR-125a-5p and miR-181c, significantly reduced macrophage CD163 expression through two distinct mechanisms. Neither microRNA was elevated in M(IL-10) with robust CD163 expression, but were instead induced in M(LPS+IC) where they restricted CD163 mRNA expression. Mir-181 species directly targeted CD163 mRNA for degradation. In contrast, transcriptome analysis of miR-125a-5p overexpression identified “cytokine-cytokine receptor interactions” as the most significantly repressed gene pathway, including decreased IL10RA, which is required for IL-10-mediated CD163 expression. Finally, overexpression of miR-181c inhibited CD163 anti-inflammatory responses to hemoglobin or high mobility group box 1 complexes. Together, these data show that microRNA utilize multiple mechanisms to integrate well characterized polarization phenotypes and regulate macrophage functional properties seen in SJIA.

2018-04-12 | GSE104853 | GEO

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

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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

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