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Mechanical checkpoint regulates monocyte differentiation in fibrotic niches.

ABSTRACT: Mechanical checkpoint regulates monocyte differentiation in fibrotic niches.

PROVIDER: PRJNA852088 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19794123.fastq.gz	Fastqsanger.gz
	SRR19794124.fastq.gz	Fastqsanger.gz
	SRR19794125.fastq.gz	Fastqsanger.gz
	SRR19794126.fastq.gz	Fastqsanger.gz
	SRR19794127.fastq.gz	Fastqsanger.gz

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Mechanical checkpoint regulates monocyte differentiation in fibrotic niches.

Project description:Myelofibrosis is a progressive bone marrow malignancy associated with monocytosis, and is believed to promote the pathological remodelling of the extracellular matrix. Here we show that the mechanical properties of myelofibrosis, namely the liquid-to-solid properties (viscoelasticity) of the bone marrow, contribute to aberrant differentiation of monocytes. Human monocytes cultured in stiff, elastic hydrogels show proinflammatory polarization and differentiation towards dendritic cells, as opposed to those cultured in a viscoelastic matrix. This mechanically induced cell differentiation is blocked by inhibiting a myeloid-specific isoform of phosphoinositide 3-kinase, PI3K-γ. We further show that murine bone marrow with myelofibrosis has a significantly increased stiffness and unveil a positive correlation between myelofibrosis grading and viscoelasticity. Treatment with a PI3K-γ inhibitor in vivo reduced frequencies of monocyte and dendritic cell populations in murine bone marrow with myelofibrosis. Moreover, transcriptional changes driven by viscoelasticity are consistent with transcriptional profiles of myeloid cells in other human fibrotic diseases. These results demonstrate that a fibrotic bone marrow niche can physically promote a proinflammatory microenvironment.

| S-EPMC10197159 | biostudies-literature

Mechanical checkpoint regulates monocyte differentiation in fibrotic niches.

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

2022-07-11 | GSE206773 | GEO

2 integrins impose a mechanical checkpoint on macrophage phagocytosis

Project description:Phagocytosis is an intensely physical process that depends on the mechanical properties of both the phagocytic cell and its chosen target. Here, we employed differentially deformable hydrogel microparticles to examine the role of cargo rigidity in the regulation of phagocytosis by macrophages. Whereas stiff cargos elicited canonical phagocytic cup formation and rapid engulfment, soft cargos induced an architecturally distinct response, characterized by filamentous actin protrusions at the center of the contact site, slower cup advancement, and frequent phagocytic stalling. Using phosphoproteomics, we identified 2 integrins and their downstream effectors as critical mediators of this mechanically regulated phagocytic switch. Indeed, comparison of wild type and 2 integrin deficient macrophages indicated that integrin signaling acts as a mechanical checkpoint by shaping filamentous actin to enable distinct phagocytic engulfment strategies. Collectively, these results illuminate the molecular logic of leukocyte mechanosensing and reveal potential avenues for modulating phagocyte function in immunotherapeutic contexts.

2024-08-22 | PXD049434 | Pride

Three Distinct Cell Types Express Extracellular Matrix Proteins In Different Niches During Skeletal Muscle Fibrosis

Project description:Tissue extracellular matrix provides structural support and creates unique niches for resident cells . However, the identities of cells responsible for creating specific ECM niches have not been determined. In striated muscle, the identity of these cells becomes important in disease when ECM changes result in fibrosis and subsequent increased tissue stiffness and dysfunction. Here we describe a novel approach to isolate and identify cells that maintain ECM niches in both healthy and fibrotic muscle. Using a collagen I reporter mouse, we show that there are three distinct cell populations that express collagen I in both healthy and fibrotic skeletal muscle. Interestingly, the number of collagen I expressing cells in all three cell populations increase proportionally in fibrotic muscle indicating that all cell types participate in the fibrosis process. Furthermore, it is shown that the ECM gene expression profile is not qualitatively altered in fibrotic muscle. This suggests that muscle fibrosis in this model results from an increased number of collagen I expressing cells and not the initiation of a specific fibrotic gene expression program. Finally, in fibrotic muscle, we show that these collagen I expressing cell populations differentially express distinct ECM proteins – fibroblasts express the fibrillar components of ECM, fibro/adipogenic progenitors cells differentially express basal laminar proteins and skeletal muscle progenitor cells differentially express genes important for the satellite cell niche.

2016-12-04 | GSE89633 | GEO

Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [Osr2KO_vs_WT_scRNA_CD8]

Project description:Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [Osr2KO_vs_WT_scRNA_CD8]

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Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [YODA1_vs_DMSO_ATAC_CD8]

Project description:Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [YODA1_vs_DMSO_ATAC_CD8]

| PRJNA925157 | ENA

Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [Osr2OE_vs_Vector_RNA_CD8]

Project description:Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [Osr2OE_vs_Vector_RNA_CD8]

| PRJNA925162 | ENA

Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [Osr2OE_vs_Vector_ATAC_CD8]

Project description:Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [Osr2OE_vs_Vector_ATAC_CD8]

| PRJNA925163 | ENA

Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [YODA1_vs_DMSO_RNA_CD8]

Project description:Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [YODA1_vs_DMSO_RNA_CD8]

| PRJNA925164 | ENA

Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [TIL_scRNA_CD8]

Project description:Osr2 functions as a mechanical checkpoint to augment CD8+ T cell exhaustion [TIL_scRNA_CD8]

| PRJNA925165 | ENA

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