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TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (scRNA-Seq)

ABSTRACT: TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (scRNA-Seq)

PROVIDER: PRJNA875139 | ENA |

REPOSITORIES: ENA

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TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration

Project description:TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration

| PRJNA875133 | ENA

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (RNA-Seq)

Project description:TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (RNA-Seq)

| PRJNA875138 | ENA

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (RNA-Seq)

Project description:IFNγ is traditionally known as a pro-inflammatory cytokine with diverse roles in antimicrobial and antitumor immunity. Yet, findings regarding its sources and functions during the regeneration process following a sterile injury are conflicting. Here, we show that natural killer (NK) cells are the main source of IFNγ in regenerating muscle. Beyond this cell population, IFNγ production is limited to a small population of T cells. We further show that NK cells do not play a major role in muscle regeneration following an acute injury or in dystrophic mice. Surprisingly, the absence of IFNγ per se also has no effect on muscle regeneration following an acute injury. However, the role of IFNγ is partially unmasked when TNFα is also neutralized, suggesting a compensatory mechanism. Using transgenic mice, we showed that conditional inhibition of IFNGR1 signaling in muscle stem cells or fibro-adipogenic progenitors does not play a major role in muscle regeneration. In contrast to common belief, we found that IFNγ is not present in the early inflammatory phase of the regeneration process, but rather peaks when macrophages are acquiring an anti-inflammatory phenotype. Our further transcriptomic analysis suggests that IFNγ cooperates with TNFα to regulate the transition of macrophages from pro- to anti-inflammatory. The absence of the cooperative effect of these cytokines on macrophages, however, does not result in significant regeneration impairment likely due to the presence of other compensatory mechanisms. Our findings support the arising view of IFNγ as a pleiotropic inflammatory regulator rather than an inducer of the inflammatory response.

2022-10-25 | GSE212372 | GEO

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration (scRNA-Seq)

2022-10-25 | GSE212371 | GEO

Mouse trophoblast cells have attenuated responses to TNFα and IFNγ that allow them to avoid synergic cytotoxicity of the two cytokines

Project description:TNFα and IFNg are two inflammatory cytokines that play critical roles in immune responses, but they can also negatively affect cell proliferation and viability. In particular, the combination of the two cytokines (TNFα/IFNγ) synergistically causes death in many cell types. We recently demonstrated that, mouse embryonic stem cells (ESCs) isolated from the inner cell mass of the blastocyst stage embryo, do not respond to TNFα and IFNg, thereby avoiding TNFα/IFNγ cytotoxicity. This study expanded our investigation to mouse trophoblast stem cells (TSCs) and differentiated trophoblasts (TSC-TBs), the major cellular constituents in trophectoderm of the blastocyst. We report here that TNFα or IFNγ alone has limited negative effect on the viability of mouse fibroblasts, but TNFα/IFNγ effectively kill these cells. However, TSCs and TSC-TBs are markedly resistant to the cytotoxicity of TNFα/IFNγ. With molecular and cellular approaches and transcriptomic analysis, we demonstrated that TSCs and TSC-TBs have attenuated responses to TNFα and IFNγ and the underlying molecular mechanisms that allow these cells to avoid the synergistic cytotoxicity of TNFα/IFNγ. Together with our previous findings in ESCs, we propose that the attenuated responses of TSCs, TSC-TBs, and ESCs to TNFα and IFNγ may serve as a protective mechanism that limits cytokine cytotoxicity in the blastocyst.

2023-11-10 | GSE224755 | GEO

TNFα and IFNγ cooperate for efficient pro- to anti-inflammatory transition of macrophages during muscle regeneration

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

2022-10-25 | GSE212373 | GEO

MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation (part 1)

Project description:Here, we investigated the time-course changes in the pattern of microRNA (miRNA) expression of TNFα and IFNγ-stimulated and unstimulated hCMEC/D3 cells, an immortalized human cerebral microvascular endothelial cell line. In order to investigate pro-inflammatory cytokine-induced changes in miRNA levels in hCMEC/D3 cells, we challenged brain endothelial cells with TNFα and IFNγ (100 ng/ml) for 2 h, 6 h and 24 h and determined microRNA expression in cytokine-stimulated and unstimulated cells

2014-04-29 | E-GEOD-44692 | biostudies-arrayexpress

Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

Project description:To investigate the impact of a pro-inflammatory stimulus (TNFα and IFNγ, 20 ng/ml) on miRNA in SCAP-EV, we isolated EV from non-activated and activated SCAP and then extracted miRNA

2022-07-20 | GSE208577 | GEO

Corticosteroid Sensitivity and the Effect of Th1 and Th17 Cytokines on Gene Expression in Human Airway Smooth Muscle

Project description:Purpose: Using RNA-sequencing, determine the effect of corticosteroids on human airway smooth muscle cells (ASM) exposed to Th1 and/or Th17 cytokines. Effects of cytokines and/or corticosteroids on gene expression was assessed. Methods: Pediatric human ASM (ages 0-21; n=4/treatment group) were serum starved for 48 h and then treated with 10 ng/mL TNFα, IFNγ, IL-17A, TNFα/IFNγ, or IFNγ/IL-17A in the presence of vehicle (0.01% DMSO) or 10 nM fluticasone propionate (FP). Cells were harvested after 18 h for RNA isolation, QC, library prep, and RNA sequencing on the Illumina HiSeq4000 platform. RNA quality and integrity was determined by gel electrophoresis and Agilent 2100 Bioanalyzer. Following sequencing. FASTQ files were processed and analyzed to generate counts files and perform differential expression analysis. Results: Our analyses show that cytokines, particularly TNFα, IFNγ, and TNFα/IFNγ had significant effects on gene expression. Differentially expressed genes were largely related to pro-inflammatory responses. Interestingly, we found that IL-17A had only modest effects on gene expression. Corticosteroids (FP) reduced or inhibited the effects of pro-inflammatory cytokines. However, these anti-inflammatory effects were reduced in cells treated with TNFα/IFNγ or IL-17A/IFNγ. Conclusions: These studies highlight the differential effects of pro-inflammatory cytokines and corticosteroids on gene expression in human ASM.

2022-05-25 | GSE179354 | GEO

Intrinsic and extrinsic mechanisms cooperate to ensure efficient termination of RNAPIII transcription.

Project description:Intrinsic and extrinsic mechanisms cooperate to ensure efficient termination of RNAPIII transcription.

| PRJNA731364 | ENA