Macrophage response to extracellular ADP stimulation
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PROVIDER: PRJNA644410 | ENA |
REPOSITORIES: ENA
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Project description:The gene expression analysis of bone marrow-derived macrophages (BMDM) treated with 100uM ADP was employed. Extracellular ADP is a danger signal that induces immune responses. Results provide insight into macrophage functions altered in ADP stimulation.
2020-07-07 | GSE153888 | GEO
Project description:The innate immune response relies on efficient, robust and fast protein signaling networks to relay information related to pathogen or viral detection. This communication is mediated primarily through protein-protein interactions and post-translational modifications (PTMs), events which are best characterized by mass spectrometry (MS)-based proteomics. This in-depth study uses MS to identify changes in protein signaling networks of Lipopolysaccharide (LPS)-stimulated human and mouse macrophages, at the level of single PTMs (via phosphorylation and ADP-ribosylation site ID) and protein complexes (via size exclusion chromatography and immunoprecipitation). The result is a curated meta-database of 6,475 proteins including 2,311 ADP-ribosylated proteins and 2,284 phosphoproteins present in LPS-stimulated macrophages. Follow up studies characterized the ASK protein complex – which appeared to dissociate upon LPS stimulation – and a complex which formed upon LPS stimulation and contained the poly(ADP-ribosyl) transferase PARP9 protein.
2020-06-17 | PXD016469 | Pride
Project description:Extracellular vesicle labeled Granulocyte macrophage progenitors
| PRJNA525660 | ENA
Project description:Molecular Pathways and Transcriptional Networks Involved in the Macrophage Response to LPS, poly(I:C) and CpG DNA Stimulation Background: Toll-like family of receptors recognizes pathogen-associated molecular patterns (PAMPs) from different organisms. TLR4 is the receptor for bacterial lipopolysaccharide (LPS), dsRNA viral mimic poly(I:C) binds to TLR3, and bacterial CpG DNA signals through TLR9. TLR4 signaling is mediated by adaptor molecules Myd88 and TRIF while TLR3 pathway involves only the TRIF adaptor and TLR9 signals solely through Myd88. Methods: To identify genes other than those in TLR pathways that mediate macrophage response to different PAMPs, RAW264.7 cells were stimulated with LPS, poly(I:C), or CpG DNA, and RNA was profiled on microarrays 6 hrs and 24 hrs post-treatment. Gene expression data were analyzed to determine genes, pathways and transcriptional networks that are in common and unique to each of the three TLR stimuli. Potentially novel candidates revealed by this analysis were tested for their role in innate immunity using RNA interference. Results: Many genes are differentially regulated by LPS and poly(I:C) at both 6 hrs and 24 hrs following treatment, while CpG DNA elicits a much less pronounced transcriptional response. By analyzing gene expression data for networks and pathways, we prioritized differentially expressed genes that are in common to all three PAMPs as well as those shared by LPS and poly(I:C). Knockdown by RNA interference of two genes, Plec1 and TPST1, inhibited production of IL-6 in response to LPS in cultured macrophages. Conclusions: We have identified novel innate immunity genes that may be important in macrophage response to LPS, poly(I:C), and CpG DNA stimuli. Our results provide potential biomarkers and therapeutic targets that should be further investigated in mice and human populations. For each treatment (LPS, polyIC, CpG DNA, media only), three biological replicates (separate macrophage cultures and RNA isolations) were profiled. Each sample was labeled with Cy3 and Cy5 and co-hybridized with Stratagene Universal Mouse Reference (dye flip techical replicates). Expression at 2 timepoints (6 and 24 hours post-treatment) was assessed.
2009-06-30 | E-GEOD-15066 | biostudies-arrayexpress
Project description:ADP array data, comprised of 2217 samples of Asian ancestry (excluding the Japanese population from ADP). Samples were genotyped on different Illumina or Affy platform.
| EGAD00010001491 | EGA
Project description:Molecular Pathways and Transcriptional Networks Involved in the Macrophage Response to LPS, poly(I:C) and CpG DNA Stimulation Background: Toll-like family of receptors recognizes pathogen-associated molecular patterns (PAMPs) from different organisms. TLR4 is the receptor for bacterial lipopolysaccharide (LPS), dsRNA viral mimic poly(I:C) binds to TLR3, and bacterial CpG DNA signals through TLR9. TLR4 signaling is mediated by adaptor molecules Myd88 and TRIF while TLR3 pathway involves only the TRIF adaptor and TLR9 signals solely through Myd88. Methods: To identify genes other than those in TLR pathways that mediate macrophage response to different PAMPs, RAW264.7 cells were stimulated with LPS, poly(I:C), or CpG DNA, and RNA was profiled on microarrays 6 hrs and 24 hrs post-treatment. Gene expression data were analyzed to determine genes, pathways and transcriptional networks that are in common and unique to each of the three TLR stimuli. Potentially novel candidates revealed by this analysis were tested for their role in innate immunity using RNA interference. Results: Many genes are differentially regulated by LPS and poly(I:C) at both 6 hrs and 24 hrs following treatment, while CpG DNA elicits a much less pronounced transcriptional response. By analyzing gene expression data for networks and pathways, we prioritized differentially expressed genes that are in common to all three PAMPs as well as those shared by LPS and poly(I:C). Knockdown by RNA interference of two genes, Plec1 and TPST1, inhibited production of IL-6 in response to LPS in cultured macrophages. Conclusions: We have identified novel innate immunity genes that may be important in macrophage response to LPS, poly(I:C), and CpG DNA stimuli. Our results provide potential biomarkers and therapeutic targets that should be further investigated in mice and human populations.
2009-07-01 | GSE15066 | GEO
Project description:Extracellular targeted protein degradation (eTPD) systems typically function through passive endocytic trafficking mechanisms that direct extracellular proteins toward lysosomal degradation without actively modulating the functional state of the target cell. Here we report macrophage-augmenting targeted chimaeras (MATACs), a dual-effector eTPD platform inspired by macrophage-mediated efferocytosis. MATACs are constructed by conjugating target-binding antibodies with synthetic polyphosphoserine (PPS) polymers that mimic the polyvalent phosphatidylserine "eat-me" signals displayed on apoptotic cells. We show that PPS functions as a programmable macrophage-targeting ligand that induces macrophage-specific uptake, lysosomal activation, and M2-like immune repolarization. By leveraging this biology, MATACs simultaneously direct extracellular and membrane-associated proteins toward macrophage lysosomes for degradation while actively reprogramming the engulfing macrophages into enhanced degradative and anti-inflammatory states. We show that MATACs efficiently degrade multiple inflammatory targets, including tumor necrosis factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), matrix metalloproteinase-9 (MMP-9), CD86, and CD40. Mechanistically, PPS engagement promotes feed-forward enhancement of macrophage phagocytic and lysosomal functions, establishing a self-amplifying degradation cascade distinct from existing eTPD systems. In murine models of rheumatoid arthritis and ulcerative colitis, TNF-alpha-targeted MATACs exhibit potent therapeutic efficacy, superior suppression of inflammatory signaling, and restoration of immune homeostasis relative to the conventional neutralizing antibody. Collectively, these findings establish MATACs as the first dual-effector extracellular degrader platform in which the effector ligand itself actively reprograms the degradative immune cell during target elimination.
2026-06-22 | GSE336034 | GEO
Project description:PTM proteomics had been increasingly used in studies related to inflammation and immunity, but the integrated analysis of multiple PTM was lacking. Here, we integrated WCP, acetylome, phosphoproteome and ubiquitinome datasets to identify LPS stimulation-dependent PTM events in macrophages with or without MG132. Using the SILAC quantification, we successfully identified 53,785 PTM sites and 19,726 proteins at all times in LPS-stimulated macrophages. Integration of these datasets provided a possibility to have a more comprehensive understanding of the inflammatory response.
| PXD015527 |
Project description:Mycobacterium tuberculosis and macrophage response
| PRJNA100713 | ENA
Project description:Bedaquiline remodels the macrophage response
| PRJNA550090 | ENA