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MCTR3 reprograms arthritic monocytes to upregulate Arginase-1 and exert pro-resolving and tissue-protective functions in experimental arthritis

ABSTRACT: We aim to demonstrate that pro-resolving mediator maresin conjugate in tissue regeneration 3 (MCTR3) potently regulates join arthritic inflammation as well as bone and cartilage repair.

ORGANISM(S): Mus musculus

PROVIDER: GSE174118 | GEO | 2022/03/31

REPOSITORIES: GEO

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MCTR3 reprograms arthritic monocytes to upregulate Arginase-1 and exert pro-resolving and tissue-protective functions in experimental arthritis

Project description:MCTR3 reprograms arthritic monocytes to upregulate Arginase-1 and exert pro-resolving and tissue-protective functions in experimental arthritis

| PRJNA728454 | ENA

Maresin 1 attenuates neuroinflammation in a mouse model of perioperative neurocognitive disorders

Project description:Maresin 1 administered to mice prior to orthopedic surgery exerts distinct anti-inflammatory and pro-resolving effects through regulation of MΦ infiltration, NF-κB signaling, and cytokine release. We used microarrays to detail the global programme of gene expression underlying Maresin 1 effect on mouse hippocampus and identified distinct classes of dysregulated genes during this process.

2018-11-13 | GSE115440 | GEO

Transcription profiling of human arthritic TNF treated synoviocytes

Project description:Time series of human arthritic synoviocytes treated with TNFalpha.

2008-06-13 | E-GEOD-516 | biostudies-arrayexpress

Maresin 1 Repletion Improves Muscle Regeneration After Volumetric Muscle Loss

Project description:The acute traumatic or surgical loss of skeletal muscle, known as volumetric muscle loss (VML), is a devastating type of injury that results in exacerbated and persistent inflammation followed by fibrosis. The mechanisms that mediate the magnitude and duration of the inflammatory response and ensuing fibrosis after VML remain understudied, and as such, the development of regenerative therapies has been limited. To address this need, we profiled how lipid mediators, which are potent regulators of the immune response after injury, varied with VML injuries that heal or result in fibrosis. We observed that non-healing VML injuries displayed increased pro-inflammatory eicosanoids and a lack of pro-resolving lipid mediators. Treatment of VML with a pro-resolving lipid mediator synthesized from docosahexaenoic acid, called Maresin 1, ameliorated fibrosis through reduction of neutrophils and macrophages and enhanced recovery of muscle strength. These results expand our knowledge of the dysregulated immune response that develops after VML and identify a novel immuno-regenerative therapeutic modality in Maresin 1.

2024-01-18 | GSE215808 | GEO

Differential gene expression of Kit+Sca1+Lin- (KSL) cells from arthritic versus control mice

Project description:The involvement of mature hematopoietic cells in disease pathogenesis is well recognized. However it is not clear how if and how primitive progenitors might contribute to inflammatory disease processes. This microarray experiment is used together with data from functional assays to determine how primitive progenitors are altered in a mouse model of autoimmune arthritis and how this in turn might contribute to the disease process. KSL cells were FACS sorted from 7 to 9 6-7 week old arthritic (KRNxG7) mice as well as from two strains of non-arthritic age-matched control mice: KRN and B6xG7 mice. Cells were sorted using identical conditions and identical sorting gates. To verify the primitive status of the KSL cells, Lin+ cells were also MACS sorted from these same mice. All the mice used in this study were C57BL/6 background strain. G7 mice are congenic with C57BL/6 but with MHC II I-Ab replaced with MHC II I-Ag7.

2012-12-31 | E-GEOD-39458 | biostudies-arrayexpress

Generation of resolving neutrophils with 4-PBA or genetic deletion of TRAM

Project description:We have generated resolving neutrophils with anti-inflammatory potency, through applying the pharmacological agent 4-PBA or genetically depleting TRAM molecule. WT murine neutrophils treated with PBS or 4-PBA for overnight were harvested for scRNAseq analysis to examine the generated resolving neutrophil phenotype. In addtion, we have cultured WT and TRAM KO neutrophils and compared the resolving phenotype via scRNAseq analysis.

2022-04-20 | GSE182356 | GEO

PROTEIN PROFILING OF AIA RAT JOINTS IN RESPONSE TO ANTI-ARTHRITIC THERAPY

Project description:Troxerutin (TXR), a potent antioxidant compound shows anti-inflammatory activity and possesses hepatoprotective effect. In this study, we aimed to exploit its anti-arthritic properties using adjuvant induced arthritic model. Using relative quantitative proteomics approach, we also tried to understand the mode of action of TXR at mechanistic details and its possible usage in the treatment of arthritis. Results provide a set of candidate biomarkers for responses to TXR in the arthritis and suggest new modalities of anti-arthritic activities. A number proteins were identified from the joint homogenates of the experimental rats using isobaric tag for relative and quantitative proteomics (iTRAQ) method. The detailed study and validation of these proteins involved may be useful in finding out newer treatment modalities.

| MSV000080172 | MassIVE

Specialized Pro-resolving Mediators Regulate Treg Differentiation

Project description:We aim to demonstrate a central role for omega-3 derived autacoids, termed specialized pro-resolving mediators (SPM), in the differentiation and maturation of Tregs.

2021-06-10 | GSE140750 | GEO

RNA sequencing in arthritic joints of wild type and Sema3B deficient mice

Project description:We found that the severity of the K/BxN serum-transfer arthritis model is higher in Sema3B deficient (Sema3b-/-) mice. Here we analyzed by RNAseq the tranciptional differences in the joints of these mice group. We used four groups: 1) WT control (non-arthritic); 2) Sema3b-/- control; 3) WT arthritis day 9; 4) Sema3b-/- artritis day 9.

2021-12-31 | GSE184782 | GEO

Study of human macrophage reprogramming toward a pro-resolving profile by efferocytosis

Project description:Inﬂammation is a physiopathological process triggered by infection or tissue damage. Immune system initiates coordinated sequential steps in response to these danger signals. Once the threat has been contained inflammation has to be subsequently shut down. Inflammation resolution is initiated by the reprogramming of pro-inflammatory macrophages toward a pro-resolving profile. This reprogramming is induced in particular by the non-phlogistic engulfment of apoptotic cells, mostly apoptotic neutrophils, a process called efferocytosis. As a matter of fact, macrophages are an essential linchpin regulating both inflammation triggering and sustaining and inflammation resolution. This duality can be achieved through the tremendous plasticity of these innate immune cells. Indeed, depending on microenvironmental signals (cytokines, efferocytosis, growth factors…) macrophages can adopt numerous diverse and sometimes antagonistic phenotypes. The mechanisms governing these transitions remain relatively scattered especially in human. With this project we propose to explore the mechanisms involved in human macrophage reprogramming toward a pro-resolving profile after efferocytosis. The stakes are high due to the estimated prevalence of chronic inflammatory diseases in Western society is 5 to 7%. Chronic inflammation is a burden to patient due to life-long debilitating illness and increased mortality and is also a burden to society due to high costs for therapy and care. Finding new therapies to limit chronic inflammation establishment and persistence is thus a highly valuable goal.

2021-12-01 | E-MTAB-8885 | biostudies-arrayexpress

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