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Macrophage GIT1 contributes to bone regeneration by regulating inflammatory response

ABSTRACT: Macrophage GIT1 contributes to bone regeneration by regulating inflammatory response

PROVIDER: PRJNA604763 | ENA |

REPOSITORIES: ENA

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Macrophage GIT1 contributes to bone regeneration by regulating inflammatory response

Project description:To investigate the altered gene expression levels in GIT1 CKO and control macrophages in response to LPS. Each group had a biological repeat (n=3). Results provide insight into the role of GIT1 in macrophages after treated with LPS.

2020-02-05 | GSE144739 | GEO

Macrophage GIT1 Contributes to Bone Regeneration by Regulating Inflammatory Responses in an ERK/NRF2-Dependent Way.

Project description: Not available

| S-EPMC7689802 | biostudies-literature

Investigation of Bach2 function by regulating inflammatory response and heme-iron homeostasis of bone marrow macrophage.

Project description:Macrophages are central in regulating iron homeostasis. Transcription repressor Bach2 regulates by heme. Here we investigated the relationship between heme-regulated Bach2 and macrophage in bone marrow. We identified RFP-positive and negative macrophage were in bone marrow. We found that RFP-positive macrophage related with iron-heme homeostasis maintenance and RPF-negative population related with immune response. In RFP positive macrophage, we also found the lysosomal heme transporter hrg-1 was Bach2 direct target gene. Our results suggest that the function of the bone marrow macrophage alters according to expression of Bach2.

2018-09-26 | GSE79697 | GEO

The Role of WTAP in Regulating Macrophage-Mediated Osteoimmune Responses and Tissue Regeneration in Periodontitis

Project description:Periodontitis, delineated by the destruction of structures that support teeth, is predominantly propelled by intricate immune responses. Immunomodulatory treatments offer considerable promise for the management of this ailment; however, the modulation of the periodontal immune microenvironment to facilitate tissue regeneration presents a substantial biomedical challenge. Herein, our study investigates the role of Wilms' tumor 1-associating protein (WTAP), a critical m6A methyltransferase, in the immunomodulation of periodontitis and assesses its viability as a therapeutic target. We observed heightened expression of WTAP in macrophages extracted from gingival tissues impacted by periodontitis, with a strong association with M1 polarization. Via loss-of-function experiments, we demonstrated that diminishing WTAP expression precipitates a transition from M1 to M2 macrophage phenotypes amidst inflammatory conditions, thus improving the periodontal immune landscape. Further, RNA sequencing and indirect co-culture assays indicated that suppressing of WTAP expression modulates osteoimmune responses and enhances the osteogenic differentiation of bone marrow stromal cells. The local deployment of adeno-associated virus-shWTAP in murine models of periodontitis robustly validated the therapeutic promise of targeting WTAP in this disease. Collectively, our findings highlight the crucial role of WTAP in orchestrating macrophage-mediated osteoimmune responses and tissue regeneration in periodontitis, proposing novel avenues for immunotherapeutic interventions in its treatment.

2024-05-24 | GSE265968 | GEO

ERMAP improves inflammatory bowel disease by regulating macrophage and T cell functions

Project description:Background & aims: Both macrophages and T cells play a critical role in inflammatory bowel disease (IBD) development. Since our previous studies have shown that a novel immune checkpoint molecule ERMAP affects macrophage polarization and negatively regulate T cell responses, we investigated the effects of ERMAP on IBD progression in mice. Methods: Using an dextran sodium sulfate (DSS)-induced IBD mice model, knockdown of ERMAP in RAW264.7 macrophages, ERMAP gene knockout mice, and Global gene expression analysis by RNA-seq, We investigate the effect of ERMAP on IBD by regulation of T cells and macrophages, NOD-like receptor (NLR) protein family pathway in macrophages. Results: We show here that administration of ERMAP protein significantly increases the proportion of anti-inflammatory M2-type macrophages and inhibits T cell activation and proliferation in IBD mice induced by DSS. Knockdown of ERMAP in RAW264.7 macrophages reduces M2-type macrophage polarization and increases T cell responses. Adoptive transfer of macrophages from ERMAP knockout mice exacerbates DSS-induced IBD. Global gene expression analysis by RNA-seq shows that ERMAP inhibits the NLR protein family pathway in macrophages. Conclusions: Our results suggest that ERMAP protein has the potential to be used in the treatment of IBD by regulating macrophage and T cell functions.

2022-08-28 | GSE212010 | GEO

CD300f immunoreceptor contributes to peripheral nerve regeneration by the modulation of macrophage inflammatory phenotype.

Project description: Not available

| S-EPMC4531482 | biostudies-literature

Macrophage-derived cholesterol contributes to therapeutic resistance in prostate cancer

Project description:Macrophage-derived cholesterol contributes to therapeutic resistance in prostate cancer

| PRJNA747294 | ENA

Bone marrow derived macrophage vs peritoneal macrophage

Project description:Bone marrow derived macrophage vs peritoneal macrophage

| PRJNA414129 | ENA

Macrophage histone lactylation during ischemia induced-muscle regeneration [CUT&Tag]

Project description:After injury, muscles require fully functional macrophages to recover completely. During muscle regeneration, macrophages transition from a pro-inflammatory to a pro-restorative phenotype ensures the proper regeneration. Lactate is a crucial molecule for muscle-residing macrophage polarisation. Histone lactylation, a direct derivative of lactate, has been implicated in macrophage polarisation in vitro . In this work, we show for the first time that macrophages recruited to the muscle after ischemic injury modify their histone lactylome between 2 and 4 days post injury. Absolute histone lactylation levels increase significantly. Although subtly, also the genomic enrichment of H3K18la changes from 2 to 4 days post injury and this correlates with gene expression changes. Interestingly, we find that H3K18la genomic enrichment changes from day 2 to day 4 post injury are predictive for gene expression changes later in time, from day 4 to day 7, rather than being a reflection of past gene expression changes from day 1 to day 2. Our results suggest that histone lactylation dynamics are functionally important for the resolving action of macrophages during muscle regeneration.

2024-04-08 | GSE254129 | GEO

Macrophage histone lactylation during ischemia induced-muscle regeneration [RNA-Seq]

2024-04-08 | GSE254128 | GEO

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