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Microarray analysis of Mef2c deficient and control bone marrow pre-B and pro-B cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE63998 | GEO | 2016/07/12

SECONDARY ACCESSION(S): PRJNA269749

REPOSITORIES: GEO

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Microarray analysis of Mef2c deficient and control bone marrow pro-B cells

Project description:Gene expression of mice bone marrow pro-B cells from both control and Vav-Cre Mef2cfl/fl mice (9 months old) We used these microarrays to identify the function of MEF2C in BM B lymphoid progenitors

2016-07-12 | GSE63997 | GEO

Microarray analysis of Mef2c deficient and control bone marrow pre-B cells

Project description:Gene expression of mice bone marrow pre-B cells from both control and Vav-Cre Mef2cfl/fl mice (9 months old) We used these microarrays to identify the function of MEF2C in BM B lymphoid progenitors

2016-07-12 | GSE63996 | GEO

Microarray analysis of Mef2c deficient and control bone marrow pre-B and pro-B cells

Project description:Microarray analysis of Mef2c deficient and control bone marrow pre-B and pro-B cells

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Expression profiling in bone-marrow-derived neutrophils of lcn2 deficient mouse

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-31 | E-GEOD-43891 | biostudies-arrayexpress

MEF2C protects bone marrow B-lymphoid progenitors during stress haematopoiesis.

Project description:DNA double strand break (DSB) repair is critical for generation of B-cell receptors, which are pre-requisite for B-cell progenitor survival. However, the transcription factors that promote DSB repair in B cells are not known. Here we show that MEF2C enhances the expression of DNA repair and recombination factors in B-cell progenitors, promoting DSB repair, V(D)J recombination and cell survival. Although Mef2c-deficient mice maintain relatively intact peripheral B-lymphoid cellularity during homeostasis, they exhibit poor B-lymphoid recovery after sub-lethal irradiation and 5-fluorouracil injection. MEF2C binds active regulatory regions with high-chromatin accessibility in DNA repair and V(D)J genes in both mouse B-cell progenitors and human B lymphoblasts. Loss of Mef2c in pre-B cells reduces chromatin accessibility in multiple regulatory regions of the MEF2C-activated genes. MEF2C therefore protects B lymphopoiesis during stress by ensuring proper expression of genes that encode DNA repair and B-cell factors.

| S-EPMC4987520 | biostudies-literature

Microarray analysis of mouse bone marrow hematopoietic progenitors

Project description:This SuperSeries is composed of the SubSeries listed below.

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Expression profiling in bone-marrow-derived neutrophils of lcn2 deficient mouse

Project description:This SuperSeries is composed of the SubSeries listed below.

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Transcriptomic signature and pro-osteoclastic secreted factors of abnormal bone marrow stromal cells in fibrous dysplasia

Project description:This SuperSeries is composed of the SubSeries listed below.

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Bone marrow niche

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-04-10 | GSE108892 | GEO

miR-155-deficient bone marrow promotes tumor metastasis.

Project description:Infiltration of immune cells in primary tumors and metastatic sites is known to influence tumor progression and metastasis. Macrophages represent the most abundant immune cells in the tumor microenvironment, and evidence has shown that macrophages promote seeding, extravasation, and persistent growth of tumor cells at metastatic sites. miR-155 plays an essential role in immune cell development/function, and its aberrant expression is associated with lymphomas and several solid tumor types. However, it is unknown how miR-155 expression in immune cells affects solid tumor growth and metastasis. To this end, bone marrow transplantation was performed using miR-155-deficient mice as bone marrow donors and wild-type (WT) mice as recipients, and the chimeric mice were inoculated with tumor cells. We demonstrate that bone marrow lacking miR-155 significantly enhanced lung metastasis without a substantial effect on primary tumor growth. Relative to mice with WT bone marrow, miR-155-deficient bone marrow accumulated more macrophages in the spleen and lungs. Further analysis revealed that miR-155-deficient macrophages in metastatic sites exhibited a tumor-promoting M2 phenotype. In vitro study suggested that miR-155-null macrophages were prone to M2 polarization upon incubation with tumor cell-conditioned medium, due to elevated expression of C/EBP?, an identified miR-155 target. These data, for the first time, demonstrate that miR-155 in host immune cells plays a vital role in modulating solid tumor metastasis by affecting the recruitment and polarization of bone marrow-derived macrophages.Targeted inhibition of miR-155 delays tumor development but inhibition in host immune cells may encourage metastasis.

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