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Transcriptomic changes in macrophages induced by damage-associated molecular patterns (DAMPs)

ABSTRACT: Transcriptomic changes in macrophages induced by damage-associated molecular patterns (DAMPs)

PROVIDER: PRJNA632501 | ENA |

REPOSITORIES: ENA

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Transcriptomic changes in macrophages induced by damage-associated molecular patterns (DAMPs)

Project description:Dead cell-derived molecules, typically called as damage-accociated molecular patterns (DAMPs), have been shown to evoke inflammatory responses. Accordingly, it becomes increasingly clear that DAMPs play important role in pathogenesis of multiple diseases including inflammatory diseases and cancer. To get a comprihensive view of DAMP-mediated inflammatory responses, we perfomed microarray analysis on murine macrophages treated by dead cell-derived molecules.

2021-05-21 | GSE150465 | GEO

Damage-associated molecular patterns by dying cancer cells

Project description:The molecular hallmark of immunogenic cell death (ICD) features the release of damage-associated molecular patterns (DAMPs) by dying cancer cells. Herein, measuring DAMPs from gemcitabine-induced dying cancer cells, via mass spectrometry (MS) proteomic profiling.

2020-11-04 | MSV000086407 | MassIVE

Damage-associated molecular patterns (DAMPs) by dying cancer cells

2020-10-29 | MSV000086386 | MassIVE

Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

Project description:Dying cells release Damage-Associated Molecular Patterns (DAMPs) that can initiate and perpetuate sterile inflammatory responses. However, the effect of DAMPs on macrophages biology remains unclear. We therefore studied the effect of DAMPs on primary peritoneal macrophages (PPM) in vitro. We first performed unbiased transcriptomic profiling with RNA-seq of PPMs cultured for up to 72 hours in the presence and absence of: 1) liposaccharide (LPS), which is known to provoke an “M1” phenotype, 2) IL-4, which is known to provoke an “M2” phenotype, or 3) cytosolic extracts (CEs) from necrotic H9C2 cells to mimic the release of cardiomyocyte DAMPs. We found that the transcriptional profile of PPMs stimulated with CEs resembled the transcriptional profile of PPMs stimulated with LPS.

2019-08-21 | GSE107776 | GEO

Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

Project description:Damage-associated molecular patterns induce macrophage polarization toward an M1 pro-inflammatory phenotype

| PRJNA421349 | ENA

Changes of Damage Associated Molecular Patterns in COVID-19 Patients

Project description: Not available

| S-EPMC8057315 | biostudies-literature

DNA damage responses activate a multi-functional genetic program in murine bone marrow-derived macrophages

Project description:DNA damage response kinase ATM regulates the genetic program of lymphocytes with phsiologically induced DNA DSBs. In bone marrow-derived macrophages, related kinase DNAPKcs is also responsible for activating DNA damage responses after infection with Listeria monocytogenes. Here we show that both ATM and DNA-PKcs regulate the genetic program of Listeria monocytogenes-infected macrophages. Two independent bone marrow-derived macrophage cultures for each genotype (LysMcre/+ and Scid: Atmc/c: LysMcre/+) were infected with Listeria monocytogenes for 24 hrs at an MOI of 5. RNA was isolated using RNeasy (Qiagen). Gene expression profiling was performed using Illumina MouseRef-8 expression microarrays.

2015-07-03 | E-GEOD-70467 | biostudies-arrayexpress

DNA damage responses activate a multi-functional genetic program in murine bone marrow-derived macrophages

2015-07-03 | GSE70467 | GEO

Caspase-dependent cell death-associated release of nucleosome and damage-associated molecular patterns.

Project description: Not available

| S-EPMC4649531 | biostudies-other

The Cellular and Molecular Origin of Tumor-associated Macrophages

Project description:Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered as regulators of several diseases including cancer. Here we show that in mice, mammary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypically and functionally distinct from mammary tissue macrophages (MTMs). TAMs express the adhesion molecule Vcam1 and proliferate upon their differentiation from inflammatory monocytes, but do not exhibit an “alternatively activated” phenotype. TAM differentiation depends on the transcriptional regulator of Notch signaling, RBPJ; and TAM, but not MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth. These findings reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response, which may provide new opportunities for cancer immunotherapy. MMTV-PyMT mice (Jackson Laboratory) were backcrossed to the C57BL/6 background for 10 generations. Rbpjfl/fl mice were provided by Tasuku Honjo and crossed to CD11ccre mice provided by Boris Reizis. Littermate controls were used in all experiments when possible. All mice were maintained in a specific pathogen-free facility and animal experimentation was conducted in accordance with institutional guidelines. In the MMTV-PyMT spontaneous mammary tumor model, we found the key Notch transcriptional regulator, RBPJ, to be required for TAM terminal differentiation from inflammatory monocytes. The bulk myeloid cell population that remains in CD11cCreRbpj fl/fl mice (the cells in "Rbpj KO" samples), represents monocytes that have begun their differentiation into macrophages, but are unable to terminally differentiate due to the lack of Rbpj.

2014-04-18 | E-GEOD-56755 | biostudies-arrayexpress

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