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Targeting macrophage M1 polarization suppression through PCAF inhibition alleviates autoimmune arthritis via synergistic NF-κB and H3K9Ac blockade

ABSTRACT: M1 macrophages are considered to contribute to autoimmune arthritis such as rheumatoid arthritis, spondyloarthritis. However, the exact role of M1 macrophage during inflammatory joint disease remain unclear. To explore the molecular mechanisms underlying M1 macrophage in autoimmune arthritis, we performed the whole transcriptome sequencing of 3 repeats of M0, 3 repeats of M1 without 20 μM Garcinol and 3 repeats of M1 with 20 μM Garcinol.

ORGANISM(S): Homo sapiens

PROVIDER: GSE221012 | GEO | 2022/12/20

REPOSITORIES: GEO

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Targeting macrophage M1 polarization suppression through PCAF inhibition alleviates autoimmune arthritis via synergistic NF-κB and H3K9Ac blockade

Project description:Targeting macrophage M1 polarization suppression through PCAF inhibition alleviates autoimmune arthritis via synergistic NF-κB and H3K9Ac blockade

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Proteomic Identification of Interferon-induced Proteins with Tetratricopeptide Repeats (IFITs) as Markers of M1 Macrophage Polarization

Project description:Proteomic studies of macrophage polarization to pro-inflammatory (M1) or tissue reparative (M2) phenotypes has identified interferon-induced proteins with tetratricopeptide repeats (IFIT1, IFIT2 and IFIT3) as potential biomarkers of inflammatory diseases such as atherosclerosis.

2018-03-15 | PXD008204 | Pride

Transcriptomic and proteomic profiling of non-classical monocytes unravels distinct pathogenic features in SLE

Project description:Current non-specific immunosuppressive treatments for Systemic Lupus Erythematosus (SLE) show modest efficacy. In SLE the monocytic/macrophage (Mo/Mφ) system plays a key role in the initiation and perpetuation of the systemic autoimmune response. However, the distinct functions of the Mo/Mφ cellular subsets remain elusive. Herein, we demonstrate a distinct proteomic and transcriptomic profile of non-classical monocytes (NCM) of active patients with SLE with enhanced inflammatory features such as deregulated DNA repair, cell cycle and enhanced IFN signaling in parallel with cell differentiation and developmental cues. Ex-vivo assays revealed an upregulation of p53 due to enhanced DNA damage along with G0 cell cycle arrest of SLE NCM indicative of an inflammatory phenotype. This aberrant profile of NCM of active patients with SLE is linked with an activated macrophage-like and enriched M1 pro-inflammatory response. We envisage that enhanced autophagy in SLE NCM may drive their differentiation towards an M1-like macrophage profile contributing to disease severity. Together, these findings provide evidence of skewed differentiation of NCM towards an M1-like macrophage phenotype as a pathogenic feature of NCM in SLE.

2023-11-21 | PXD042539 | Pride

Gene expression data from murine M1 and M2 macrophages

Project description:Macrophages have distinct characteristics depending on their microenvironment. We performed proteomic analysis between M1 and M2 macrophages and found that cellular metabolism is the key regulator of macrophage function. We used microarray to support proteomic data between M1 and M2 macrophages. M1 macrophages are obtained using cell sorting of CD45+MHCII+CD8a-F4/80+ population from C57BL/6J bone marrow cell derived heterogenous cells under GM-CSF conditioning for 7 days. M2 macrophages are differentiated with 20% L929 cell supernatant for 7 days and sorted from CD45+F4/80+CD11b+ population.

2014-11-14 | E-GEOD-63245 | biostudies-arrayexpress

Novel transcriptome signatures and markers defining murine macrophages at the extremes of the canonical M1 and M2 polarization spectrum

Project description:Classically (M1) and alternatively activated (M2) macrophages play distinct roles in various physiological and disease processes. Understanding the gene transcription programs that contribute to macrophage polarization along the M1/M2 spectrum may lead to new tools to detect and therapeutically manipulate macrophage phenotype. Here, we define the M1 and M2 macrophage signature through mRNA microarray. The M1 macrophage signature was defined by 629 up-regulated and 732 down-regulated genes while the M2 macrophage signature was formed by 388 up-regulated and 425 down-regulated genes. While a subset of probes was common to both M1 and M2 cells, others were exclusive to each macrophage subset. The common M1/M2 pathways were characterized by changes in various transcriptional regulators and signaling partners, including increases in Kruppel-like Factor (Klf) 4, but decreases in Klf2. To identify M1 and M2 biomarkers that help discriminate these populations, we selected genes that were increased during M1 or M2 differentiation but decreased in the opposite population. Among top novel M1-distinct genes, we identified CD38, G-protein coupled receptor 18 (Gpr18) and Formyl peptide receptor 2 (Fpr2). Among top M2 genes, we found early growth response protein 2 (Egr2) and Myc. We validated these genes by Real-Time PCR and developed a CD38/Egr2-based flow cytometry assay that discriminates between M1 and M2 macrophages. Overall, this work defines the M1 and M2 signature and identifies several novel M1 and M2 genes that may be used to distinguish and manipulate M1 and M2 macrophages. Total RNA was prepared from bone marrow-derived macrophages of wild-type mice (n=2-3 independent mice) treated in M0, M1 or M2 conditions (n=2-3 replicates per condition originating from different mice)

2015-12-08 | E-GEOD-69607 | biostudies-arrayexpress

Expression data from macrophage maturation and polarization c-Myc in alternative macrophage activation experiments

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2011-09-15 | E-GEOD-32164 | biostudies-arrayexpress

Mus musculus

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Project description:Sulforaphene inhibit M1 macrophage

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Potentiation of glucocorticoid signaling by chloroquine via inhibition of lysosomes

Project description:Anti-malaria drug chloroquine has been used as an anti-inflammatory agent for treating systemic lupus erythematosus and rheumatoid arthritis, without clear mechanism of action. Here we report that chloroquine potently inhibits the expression of proinflammatory cytokines through transrepression of glucocorticoid receptor (GR). Instead of direct binding to GR, chloroquine synergistically activates glucocorticoid signaling via inhibition of lysosomal functions. In mouse collagen induced arthritis model, chloroquine synergizes the therapeutic effects of glucocorticoid. Lysosomal inhibition by bafilomycin A1, an inhibitor of V-type ATPase, or by knockdown of transcription factor EB (TFEB), a master activator of lysosomal biogenesis, mimics the effects of chloroquine. These results reveal an unexpected regulation of glucocorticoid signaling by lysosomes and provide a mechanistic basis for treating inflammation and autoimmune diseases by combination of glucocorticoids and lysosomal inhibitors. Macrophage THP-1 cells treated with LPS, chloroquine and dexamethasone.

2012-01-18 | E-GEOD-24579 | biostudies-arrayexpress

Functional differences of experimental arthritis splenic macrophages in DA and DAMut rats are revealed by quantitative proteomics

Project description:Rheumatoid arthritis (RA) is a devastating chronic inflammatory disorder affecting 0.5-1.0% of adults worldwide and is characterized by autoimmune reactivity and persistent active inflammation with concurrent tissue destruction. Animal models of RA provide an opportunity to understand disease pathogenesis and develop new therapeutic strategies . The DA inbred rat is commonly used in autoimmunity research due to its high susceptibility to several chronic inflammatory disorders such as arthritis and experimental autoimmune encephalomyelitis (EAE). The experimental arthritis induced by pristane, the arthritogenic component in mineral oil, in the DA rat can be classified with RA criteria, including a chronic relapsing disease course 5, 6. We have identified a mutation DA rat and the mutation plays a completely protective function in DA rats against EAE and pristane-induced arthritis (PIA). Macrophages are an essential source of pro-inflammatory cytokines in chronic inflammation and the progressive destruction of synovial joints. To elucidate the molecular mechanism by which the mutation regulates macrophage activation, we made quantitative mass spectrometry on the four groups of splenic macrophages: DA-control, DAMut-control, DA-PIA, DAMut-PIA.

2023-04-04 | PXD041317 |

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