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Mesenchymal Stem Cells (MSCs) Alleviate Experimental Immune-mediated Liver Injury via Chitinase 3-like protein 1-mediated T cell suppression

ABSTRACT: Mesenchymal Stem Cells (MSCs) Alleviate Experimental Immune-mediated Liver Injury via Chitinase 3-like protein 1-mediated T cell suppression

PROVIDER: PRJNA700504 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13649620.fastq.gz	Fastqsanger.gz
	SRR13649621.fastq.gz	Fastqsanger.gz
	SRR13649622.fastq.gz	Fastqsanger.gz
	SRR13649623.fastq.gz	Fastqsanger.gz
	SRR13649624.fastq.gz	Fastqsanger.gz

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Mesenchymal Stem Cells (MSCs) Alleviate Experimental Immune-mediated Liver Injury via Chitinase 3-like protein 1-mediated T cell suppression

Project description:RNA-seq for MSCs from human bone marrow (BM-MSCs), olfactory mucosa (OM-MSCs), and umbilical cord (UC-MSCs) (2 donors for each). RNA-sequencing for human naïve CD3+ T cells, CD3+ T cells activated with PHA (2.5 μg/mL) for 48 h， and CD3+ T cells co-cultured with human UC-MSCs in the presence of PHA for 48 h.

2021-02-09 | GSE166327 | GEO

Mesenchymal stem cells alleviate experimental immune-mediated liver injury via chitinase 3-like protein 1-mediated T cell suppression.

Project description:Liver diseases with different pathogenesis share common pathways of immune-mediated injury. Chitinase-3-like protein 1 (CHI3L1) was induced in both acute and chronic liver injuries, and recent studies reported that it possesses an immunosuppressive ability. CHI3L1 was also expressed in mesenchymal stem cells (MSCs), thus we investigates the role of CHI3L1 in MSC-based therapy for immune-mediated liver injury here. We found that CHI3L1 was highly expressed in human umbilical cord MSCs (hUC-MSCs). Downregulating CHI3L1 mitigated the ability of hUC-MSCs to inhibit T cell activation, proliferation and inflammatory cytokine secretion in vitro. Using Concanavalin A (Con A)-induced liver injury mouse model, we found that silencing CHI3L1 significantly abrogated the hUC-MSCs-mediated alleviation of liver injury, accompanying by weakened suppressive effects on infiltration and activation of hepatic T cells, and secretion of pro-inflammatory cytokines. In addition, recombinant CHI3L1 (rCHI3L1) administration inhibited the proliferation and function of activated T cells, and alleviated the Con A-induced liver injury in mice. Mechanistically, gene set enrichment analysis showed that JAK/STAT signalling pathway was one of the most significantly enriched gene pathways in T cells co-cultured with hUC-MSCs with CHI3L1 knockdown, and further study revealed that CHI3L1 secreted by hUC-MSCs inhibited the STAT1/3 signalling in T cells by upregulating peroxisome proliferator-activated receptor δ (PPARδ). Collectively, our data showed that CHI3L1 was a novel MSC-secreted immunosuppressive factor and provided new insights into therapeutic treatment of immune-mediated liver injury.

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Chitinase-3-like-1 Protein Complexes Modulate Macrophage-Mediated Immune Suppression in Glioblastoma

Project description:Chitinase-3-like-1 Protein Complexes Modulate Macrophage-Mediated Immune Suppression in Glioblastoma

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Particulate Matter10-induced airway inflammation and fibrosis can be regulated by chitinase-1 suppression

Project description:Particulate matter10 (PM10) can induce airway inflammation and fibrosis. Chitinase-1 is recently known to have key roles in inflammation and fibrosis. We aimed to investigate the effects of chitinase-1 inhibitor in PM10-treated murine models. PM10 and/or OVA-induced airway inflammation and fibrosis murine models were well established. CPX and dexamethasone ameliorated PM10 or PM10/OVA-induced airway hyper-responsiveness, airway inflammation, and fibrosis. CPX and dexamethasone also reduced levels of various inflammatory markers including chitinase-1 in lung homogenates. PM10 and OVA also induced extreme changes of mRNA expression. CPX and dexamethasone decreased levels of mRNA expression especially associated with inflammation and immune regulation. They also significantly regulated asthma and asthma related pathway including JACK-STAT signaling pathway.Chitinase-1 suppression by CPX can regulate PM10-induced and aggravated airway inflammation and fibrosis via various signaling pathway.

2023-01-05 | GSE222111 | GEO

Chitinase-3-like-1 Protein Complexes Modulate Macrophage-Mediated Immune Suppression in Glioblastoma

Project description:Glioblastoma is a highly malignant and incurable brain tumor characterized by intrinsic and adaptive resistance to immunotherapies. However, how glioma cells induce tumor immunosuppression and escape immunosurveillance remains poorly understood. Here, we find upregulation of cancer-intrinsic Chitinase-3-like-1 (CHI3L1) signaling modulating an immunosuppressive microenvironment by reprogramming tumor-associated macrophages (TAMs). Mechanistically, CHI3L1 binding with Galectin-3 (Gal3) selectively promotes TAM migration and infiltration with a protumor M2-like but not an antitumor M1-like phenotype in vitro and in vivo, governed by a transcriptional program of NFκB/CEBPβ in the CHI3L1/Gal3-PI3K/AKT/mTOR axis. Conversely, Galectin-3-binding protein (Gal3BP) negatively regulates this process by competing with Gal3 to bind CHI3L1. Administration of a Gal3BP mimetic peptide in a syngeneic glioblastoma mouse model reverses immune suppression and attenuates tumor progression. These results shed light on the role of CHI3L1 protein complexes in immune evasion by glioblastoma and as a potential immunotherapeutic target for this devastating disease.

2021-05-11 | GSE174177 | GEO

Gene expression activation in CLL mediated by MSCs contact

Project description:Survival of primary CLL cells is mediated by mesenchimal stromal cells in vitro. The goal of this study is to compare the gene expression profile of primary CLL cells in monoculture to that one following cell-cell contact with MSCs

2019-05-20 | GSE99724 | GEO

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Secretome from iPSC-derived MSCs exerts proangiogenic and immunosuppressive effects to alleviate radiation-induced vascular endothelial cell damage

Project description:Secretome from iPSC-derived MSCs exerts proangiogenic and immunosuppressive effects to alleviate radiation-induced vascular endothelial cell damage

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Mesenchymal Stromal Cells Alleviate Depressive and Anxiety-like Behaviors via a Lung Vagal-to-Brain Axis in Male Mice

Project description:Major depressive disorder (MDD) is one of the most common and disabling mental disorders, and current strategies remain inadequate. Although mesenchymal stromal cells (MSCs) have shown beneficial effects in experimental models of depression, underlying mechanisms remain elusive. Here, using murine depression models, we demonstrated that MSCs could alleviate depressive and anxiety-like behaviors not due to a reduction in proinflammatory cytokines, but rather activation of dorsal raphe nucleus (DRN) 5-hydroxytryptamine (5-HT) neurons. Mechanistically, peripheral delivery of MSCs activated pulmonary innervating vagal sensory neurons, which projected to the nucleus tractus solitarius, inducing the release of 5-HT in DRN. Furthermore, MSC-secreted brain-derived neurotrophic factor activated lung sensory neurons through tropomyosin receptor kinase B (TrkB), and inhalation of a TrkB agonist also achieved significant therapeutic effects in male mice. This study reveals a role of peripheral MSCs in regulating central nervous system function and demonstrates a potential "lung vagal-to-brain axis" strategy for MDD.

2023-10-30 | GSE246290 | GEO

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