Mouse bone marrow stromal cells: before or after total body irradiation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE72235 | GEO | 2016/09/01
SECONDARY ACCESSION(S): PRJNA293444
REPOSITORIES: GEO
Similar Datasets
Project description:Comprehensive gene expression analysis in BM-resident stromal cells was performed for an overview of BM environmental change caused by total body irradiation (TBI). Total RNA samples collected from BM-resident stromal cells with or without TBI were subjected to high sensitivity DNA microarray assays Three-condition experiment: Unirradiated, 1 day after TBI and 3 days after TBI. Bone marrow stromal cells were obtained from C57BL/6 mice (n = 6) either non-irradiated or after 9.5 Gy irradiation at indicated times.
2016-09-01 | E-GEOD-72235 | biostudies-arrayexpress
Project description:A major challenge in bone allogeneic marrow (BM) transplantation is overcoming engraftment resistance to avoid the clinical problem of graft rejection. Identifying genes and pathways that regulate BM engraftment may reveal molecular targets for overcoming these engraftment barriers. Previously, we developed a mouse model of BM transplantation that utilizes recipient conditioning with non-myeloablative total body irradiation followed by transplantation of allogeneic BM cells. We defined TBI doses that lead to graft rejection, that are permissive for engraftment, and mouse strain variation with regards to the permissive TBI dose. We now report gene expression analysis, using the Agilent Mouse 8x60K v3 expression arrays, in spleen of mice conditioned with TBI doses for evaluation in correlation to the expected engraftment phenotype. The spleens of mice given TBI demonstrated extensive differential gene expression, compared with un-irradiated controls, at both multiple testing-corrected P < .05 and fold change greater than or equal to 2 levels. Functional analysis revealed significant enrichment for up-regulation of canonical pathways involved in inflammation, even when treated with TBI doses not permissive for engraftment. Consistent with this the most significantly associated upstream regulators included lipopolysaccharide, tumor necrosis factor, and a toll-like receptor. Unique to engrafting mice, however, were enrichment for a down-regulated canonical pathway related to B-cell development. Results from this analysis have identified canonical pathways and upstream regulators of BM engraftment in mice and may lead to new approaches to overcome the problem of graft rejection complicating clinical BM transplantation.
2013-01-08 | GSE43310 | GEO
Project description:A major challenge in bone allogeneic marrow (BM) transplantation is overcoming engraftment resistance to avoid the clinical problem of graft rejection. Identifying genes and pathways that regulate BM engraftment may reveal molecular targets for overcoming these engraftment barriers. Previously, we developed a mouse model of BM transplantation that utilizes recipient conditioning with non-myeloablative total body irradiation followed by transplantation of allogeneic BM cells. We defined TBI doses that lead to graft rejection, that are permissive for engraftment, and mouse strain variation with regards to the permissive TBI dose. We now report gene expression analysis, using the Agilent Mouse 8x60K v3 expression arrays, in spleen of mice conditioned with TBI doses for evaluation in correlation to the expected engraftment phenotype. The spleens of mice given TBI demonstrated extensive differential gene expression, compared with un-irradiated controls, at both multiple testing-corrected P < .05 and fold change greater than or equal to 2 levels. Functional analysis revealed significant enrichment for up-regulation of canonical pathways involved in inflammation, even when treated with TBI doses not permissive for engraftment. Consistent with this the most significantly associated upstream regulators included lipopolysaccharide, tumor necrosis factor, and a toll-like receptor. Unique to engrafting mice, however, were enrichment for a down-regulated canonical pathway related to B-cell development. Results from this analysis have identified canonical pathways and upstream regulators of BM engraftment in mice and may lead to new approaches to overcome the problem of graft rejection complicating clinical BM transplantation. Each individual sample was pooled from 3 mice and performed in triplicate for each experimental group (TBI 300 cGy, 400 cGy, or 500 cGy) and for each strain mice (BALB.K or B10.BR) for statistical analysis. Additional arrays were perfromed for TBI 800 cGy (BALB.K) and TBI 900 cGy (B10.BR) for anlaysis of gene expressive after myeloablative condition.
2013-01-08 | E-GEOD-43310 | biostudies-arrayexpress
Project description:A 2 Gy-total body irradiation (TBI) of WT mice induces a second wave of ROS and a second wave of apoptosis in hematopoietic stem cells starting from 6 days after irradiation. In CD169DTR/+ mice, which are depleted in CD169+ resident macrophages after a diphtheria toxin injection, these two waves do not occur and a total recovery of the LT-HSC pool is observed, contrarily to the LT-HSC pool from WT mice, which is decreased. Our goal is to understand why these secondary waves of apoptosis and ROS occur in LT-HSC from irradiated WT mice and not in LT-HSC from irradiated mice depleted in resident macrophages, allowing a recovery of the LT-HSC pool. We used microarrays to compare the global gene expression in LT-HSC isolated from WT and CD169DTR/+ mice 5 days after irradiation, i.e. just before both secondary waves of ROS and apoptosis occurred in WT mice.
2022-02-01 | GSE189464 | GEO
Project description:Total body irradiation (TBI) of mice using two dose rates, conventional dose rate (CDR) versus flash dose rate (FLASH), induced transient decrease of number of LT-HScs in bone marrow and a total recovery of these cells 15 days after TBI We used microarrays to detail the global programme of gene expression underlying the recovery of LT-HSCs and identified distinct classes of up or down- regulated genes according the modality of irradiation
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Project description:Duplicate hybridizations with fluorochrome switching were performed following the first two fractions of total body irradiation for accumulated doses of 1.5 Gy and 3.0 Gy. Control samples for all hybridizations were from the same patient before the beginning of treatment. Keywords: dose response
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Project description:Precise study of HSCs during regeneration has been impeded by the rarity of the HSC population and depletion of phenotypic HSCs early following genotoxic stresses, such as total body irradiation (TBI). We isolated bone marrow (BM) ckit+sca-1+lin- (KSL) cells, which are enriched for HSCs, from adult C57Bl6 mice before and at several time points following TBI, as a means to map the dynamic molecular response of HSC regeneration.
2016-04-05 | GSE79744 | GEO
Project description:NHP gene expression after 4 Gy total body irradiation.
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Project description:The population's increasing risk of acute large-scale radiological/nuclear exposures underlines the need for functional radiation biomarkers. As ionizing radiation triggers a complex response on the genome, proteome, and metabolome level, all were already reported as suitable indicators of radiation-induced damage in vitro or in animal models. We aim to analyze the blood of total-body irradiated (TBI) leukaemia patients using a mass spectrometry approach and to identify and quantify plasma proteins before and after irradiation. Combining two independent mass spectrometry approaches we identified 15 plasma proteins differing in the blood of TBI patients before and after irradiation. The majority of proteins were associated with the inflammatory responce of the immune system and with metabolism of lipids. These candidate radiation biomarkers might have implications for practical biological dosimetry.
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Project description:This clinical trial studies the side effects and best dose of giving fludarabine and total-body irradiation (TBI) together followed by a donor stem cell transplant and cyclosporine and mycophenolate mofetil in treating human immunodeficiency virus (HIV)-positive patients with or without cancer. Giving low doses of chemotherapy, such as fludarabine, and TBI before a donor bone marrow or peripheral blood stem cell transplant helps stop the growth of cancer or abnormal cells and helps stop the patient’s immune system from rejecting the donor’s stem cells. The donated stem cells may replace the patient’s immune cells and help destroy any remaining cancer cells (graft-versus-tumor effect). Sometimes the transplanted cells from a donor can also make an immune response against the body’s normal cells. Giving cyclosporine (CSP) and mycophenolate mofetil (MMF) after the transplant may stop this from happening.
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