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A novel Cpa3-Cre miR-9∆fl/∆fl mouse reveals a functional role for miR-9 in promoting a mast cell invasive phenotype via upregulation of CMA1

ABSTRACT: A novel Cpa3-Cre miR-9∆fl/∆fl mouse reveals a functional role for miR-9 in promoting a mast cell invasive phenotype via upregulation of CMA1

PROVIDER: PRJNA495507 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7993180_1.fastq.gz	Fastqsanger.gz
	SRR7993180_2.fastq.gz	Fastqsanger.gz
	SRR7993181_1.fastq.gz	Fastqsanger.gz
	SRR7993181_2.fastq.gz	Fastqsanger.gz
	SRR7993177_1.fastq.gz	Fastqsanger.gz

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A novel Cpa3-Cre; miR-9∆fl/∆fl mouse reveals a functional role for miR-9 in promoting a mast cell invasive phenotype via upregulation of CMA1

Project description:The purpose of this study was to investigate the biologic consequences of miR-9 overexpression in normal mast cells and interrogate the mechanisms by which mir-9 enhances invasion. We generated a transgenic mouse line carrying a floxed-STOP-miR-9 transgene (miR-9∆fl/∆fl) and crossed it with Cpa3-Cre transgenic mice in which Cre recombinase expression is restricted largely to mast cells and basophils, by the carboxypeptidase A3 (Cpa3) promoter. RNA-seq revealed a unique transcriptional profile associated with miR-9 overexpression in BMCMCs, notably up-regulation of mast cell-restricted proteases CMA1 and MCP6 involved in extracellular matrix remodeling. Targeting of the transcriptional corepressor SIN3A by miR-9 enhanced CMA1 expression, indicating a novel regulatory pathway through which miR-9 upregulates CMA1 expression, thereby promoting an invasive phenotype. These data support a role for miR-9 in mast cell invasive properties and provide a mechanism through which dysregulation of miR-9 in mast cells may contribute to pathologic conditions involving mast cell-mediated tissue remodeling.

2018-10-11 | GSE121076 | GEO

Murine bone marrow-derived mast cells (BMMCs) transduced with pAPM lentiviruses overexpressing miR-221 vs control overexpressing miR-221m.

Project description:Bone marrow-derived mast cells were derived from three different female C57Bl/6 mice of similar age. Cells were transduced with pAPM lentiviruses either overexpressing microRNA-221 or a non functional microRNA-221 mutant, termed miR-221m, where four point-mutations were introduced in the seed sequence of miR-221. The samples overexpressing miR-221m were used as references for the corresponding miR-221 overexpressing BMMCs from the same mouse (mouse matched reference). The experiment was performed in order to gain more insights about the molecular mechanisms underlying miR-221 effects in mast cells. Two-condition experiment, BMMC overexpressing miR-221 vs BMMC overexpressing miR-221m. Biological replicates: 3 replicates overexpressing miR-221, 3 control replicates overexpressing miR-221m.

2011-11-23 | E-GEOD-24462 | biostudies-arrayexpress

Murine bone marrow-derived mast cells (BMMCs) transduced with pAPM lentiviruses overexpressing miR-221 vs control overexpressing miR-221m.

2011-11-23 | GSE24462 | GEO

Chymase-Cre; Mcl-1fl/fl Mice Exhibit Reduced Numbers of Mucosal Mast Cells.

Project description:Mast cells (MCs) are considered as key effector cells in the elicitation of allergic symptoms, and they are essential players in innate and adaptive immune responses. In mice, two main types of MCs have been described: connective tissue MCs (CTMCs) and mucosal MCs (MMCs). However, little is known about the biological functions of MMCs, which is due to the lack of suitable models to investigate MMCs in vivo. Here, we aimed to generate a mouse model selectively deficient in MMCs. It has been previously described that Cre expressed under the control of the baboon ?-chymase promotor is predominantly localized in MMCs. Therefore, we mated ?-chymase-Cre transgenic mice with mice bearing a floxed allele of the myeloid cell leukemia sequence 1 (Mcl-1). Mcl-1 encodes for an intracellular antiapoptotic factor in MCs; hence, a selective reduction in MMCs was expected. Our results show that this new mouse model contains markedly reduced numbers of MMCs in mucosal tissues, whereas numbers of CTMCs are normal. Thus, Chm-Cre; Mcl-1fl/fl mice are a useful tool for the investigation of the pathophysiological functions of MMCs in vivo.

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Mediating effects of miR-155 on the FceRI signaling responses of mast cells

Project description:MicroRNA 155 (miR-155) has been shown to regulate the gene expression of important players of physiological and pathological processes, like hematopoietic lineage differentiation, immunity and inflammation, viral infections, cancer and cardiovascular diseases, among others. Degranulation is an event in which mast cells, upon activation of the FceRI, release their granule content rich in vasoactive amines, proteases and TNFa. Additionally activation of the receptor promotes de novo synthesis of cytokines, chemokines and growth factors. Analysis of bone marrow derived mast cells (BMMC) deficient in miR-155 showed a significant increase in FceRI mediated degranulation and in the release of cytokines like TNFa, IL-6 and IL-13. In addition miR 155-/- mice presented higher anaphylaxis reactions compared to WT mice. Gene expression analysis of BMMC was performed in order to identify intermediaries of FceRI mediated degranulation under the control of miR-155. The results indicate that miR-155 regulates negatively the expression of the regulatory subunits of the kinase PI3Kgamma, Pik3r5 (p101) and Pik3r6 (p84, p87PIKAP), involved in Ca+ influx and degranulation. Total RNA from 3 independent cultures of WT and miR-155-/- BMMC treated with anti-DNP IgE and 20 ng/ml DNP-HSA for 1hr were used to performed gene expression analysis using the Affymetrix GenechipM-BM-. Mouse Gene 1.0 ST

2014-03-20 | E-GEOD-56030 | biostudies-arrayexpress

Reduced mast cell and basophil numbers and function in Cpa3-Cre; Mcl-1fl/fl mice.

Project description:It has been reported that the intracellular antiapoptotic factor myeloid cell leukemia sequence 1 (Mcl-1) is required for mast cell survival in vitro, and that genetic manipulation of Mcl-1 can be used to delete individual hematopoietic cell populations in vivo. In the present study, we report the generation of C57BL/6 mice in which Cre recombinase is expressed under the control of a segment of the carboxypeptidase A3 (Cpa3) promoter. C57BL/6-Cpa3-Cre; Mcl-1(fl/fl) mice are severely deficient in mast cells (92%-100% reduced in various tissues analyzed) and also have a marked deficiency in basophils (58%-78% reduced in the compartments analyzed), whereas the numbers of other hematopoietic cell populations exhibit little or no changes. Moreover, Cpa3-Cre; Mcl-1(fl/fl) mice exhibited marked reductions in the tissue swelling and leukocyte infiltration that are associated with both mast cell- and IgE-dependent passive cutaneous anaphylaxis (except at sites engrafted with in vitro-derived mast cells) and a basophil- and IgE-dependent model of chronic allergic inflammation, and do not develop IgE-dependent passive systemic anaphylaxis. Our findings support the conclusion that Mcl-1 is required for normal mast cell and basophil development/survival in vivo in mice, and also suggest that Cpa3-Cre; Mcl-1(fl/fl) mice may be useful in analyzing the roles of mast cells and basophils in health and disease.

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RNA-seq of colonic tissues from Hif1a(fl/fl) and Ncr1(Cre)Hif1a(fl/fl) mice

Project description:RNA-seq of colonic tissues from Hif1a(fl/fl) and Ncr1(Cre)Hif1a(fl/fl) mice

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Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.

2018-05-01 | E-MTAB-5833 | biostudies-arrayexpress

Mediating effects of miR-155 on the FceRI signaling responses of mast cells

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RNA-seq of small intestine tissues from Hif1a(fl/fl) and Ncr1(Cre)Hif1a(fl/fl) mice

Project description:RNA-seq of small intestine tissues from Hif1a(fl/fl) and Ncr1(Cre)Hif1a(fl/fl) mice

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