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A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

ABSTRACT: A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

PROVIDER: PRJNA691672 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13423513.fastq.gz	Fastqsanger.gz
	SRR13423514.fastq.gz	Fastqsanger.gz
	SRR13423515.fastq.gz	Fastqsanger.gz
	SRR13423516.fastq.gz	Fastqsanger.gz
	SRR13423517.fastq.gz	Fastqsanger.gz

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Similar Datasets

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

Project description:A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

| PRJNA691670 | ENA

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

Project description:A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

| PRJNA756289 | ENA

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

Project description:Muscle regeneration is the result of the concerted action of multiple cell types driven by the temporarily controlled phenotype switches of infiltrating monocyte-derived macrophages. Proinflammatory macrophages transition into a phenotype that drives tissue repair through the production of effectors such as growth factors. This orchestrated sequence of regenerative inflammatory events, which we termed Regeneration-Promoting Program (RPP), is essential for proper repair. However, it is not well understood how specialized repair-macrophage identity develops in the RPP at the transcriptional level and how induced macrophage-derived factors coordinate tissue repair. Gene expression kinetics-based clustering of blood circulating Ly6Chigh, infiltrating inflammatory Ly6Chigh, and reparative Ly6Clow macrophages, isolated from injured muscle, identified the TGF-beta superfamily member, GDF-15, as a component of the RPP. Myeloid GDF-15 is required for proper muscle regeneration following acute sterile injury, as revealed by gain- and loss-of-function studies. Mechanistically, GDF-15 acts both on proliferating myoblasts and muscle-infiltrating myeloid cells. Epigenomic analyses of upstream regulators of Gdf15 expression identified that it is under the control of nuclear receptors RXR/PPARg. Finally, immune single-cell RNA-seq profiling revealed that Gdf15 is coexpressed with other known muscle regeneration-associated growth factors, and their expression is limited to a unique subpopulation of repair-type macrophages (Growth Factor-Expressing Macrophages, GFEM).

2021-10-27 | GSE164722 | GEO

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

2021-11-16 | GSE182455 | GEO

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15 [scRNA-seq]

Project description:Muscle regeneration is the result of the concerted action of multiple cell types driven by the temporarily controlled phenotype switches of infiltrating monocyte-derived macrophages. Proinflammatory macrophages transition into a phenotype that drives tissue repair through the production of effectors such as growth factors. This orchestrated sequence of regenerative inflammatory events, which we termed Regeneration-Promoting Program (RPP), is essential for proper repair. However, it is not well understood how specialized repair-macrophage identity develops in the RPP at the transcriptional level and how induced macrophage-derived factors coordinate tissue repair. Gene expression kinetics-based clustering of blood circulating Ly6Chigh, infiltrating inflammatory Ly6Chigh, and reparative Ly6Clow macrophages, isolated from injured muscle, identified the TGF-beta superfamily member, GDF-15, as a component of the RPP. Myeloid GDF-15 is required for proper muscle regeneration following acute sterile injury, as revealed by gain- and loss-of-function studies. Mechanistically, GDF-15 acts both on proliferating myoblasts and muscle-infiltrating myeloid cells. Epigenomic analyses of upstream regulators of Gdf15 expression identified that it is under the control of nuclear receptors RXR/PPARg. Finally, immune single-cell RNA-seq profiling revealed that Gdf15 is co-expressed with other known muscle regeneration-associated growth factors, and their expression is limited to a unique subpopulation of repair-type macrophages (Growth Factor-Expressing Macrophages, GFEM).

2021-11-03 | GSE161467 | GEO

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15 [scRNA-seq]

Project description:A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15 [scRNA-seq]

| PRJNA678349 | ENA

A growth factor-expressing macrophage subpopulation orchestrates regenerative inflammation via GDF-15.

Project description:Muscle regeneration is the result of the concerted action of multiple cell types driven by the temporarily controlled phenotype switches of infiltrating monocyte-derived macrophages. Pro-inflammatory macrophages transition into a phenotype that drives tissue repair through the production of effectors such as growth factors. This orchestrated sequence of regenerative inflammatory events, which we termed regeneration-promoting program (RPP), is essential for proper repair. However, it is not well understood how specialized repair-macrophage identity develops in the RPP at the transcriptional level and how induced macrophage-derived factors coordinate tissue repair. Gene expression kinetics-based clustering of blood circulating Ly6Chigh, infiltrating inflammatory Ly6Chigh, and reparative Ly6Clow macrophages, isolated from injured muscle, identified the TGF-β superfamily member, GDF-15, as a component of the RPP. Myeloid GDF-15 is required for proper muscle regeneration following acute sterile injury, as revealed by gain- and loss-of-function studies. Mechanistically, GDF-15 acts both on proliferating myoblasts and on muscle-infiltrating myeloid cells. Epigenomic analyses of upstream regulators of Gdf15 expression identified that it is under the control of nuclear receptors RXR/PPARγ. Finally, immune single-cell RNA-seq profiling revealed that Gdf15 is coexpressed with other known muscle regeneration-associated growth factors, and their expression is limited to a unique subpopulation of repair-type macrophages (growth factor-expressing macrophages [GFEMs]).

| S-EPMC8635277 | biostudies-literature

A Growth Factor-Expressing Macrophage subpopulation orchestrates regenerative inflammation via GDF-15

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

2021-10-27 | GSE164723 | GEO

Distinct Fibroblast Progenitor Subpopulation Expedites Regenerative Mucosal Healing by Immunomodulation

Project description:Distinct Fibroblast Progenitor Subpopulation Expedites Regenerative Mucosal Healing by Immunomodulation

| PRJNA900216 | ENA

GDF-15 is a biomarker of aggressiveness and is down-regulated by the mTOR inhibitor sirolimus through ATF4 and ATF5 suppression in epithelioid hemangioendothelioma.

Project description:Growth and differentiation factor-15 (GDF-15), a member of the TGF-β superfamily, exhibits elevated expression in various tumor types, often linked to disease aggressiveness. In this study, which used patient-derived xenografts and paired cell lines of epithelioid hemangioendothelioma (EHE), it was found that EHE cells produce and release GDF-15. Furthermore, the mTOR inhibitor sirolimus was observed to inhibit GDF-15 expression and release by down-regulating ATF4 and ATF5 transcription factors. To assess the clinical relevance of GDF-15 in EHE, which can manifest as both relatively indolent and exceptionally aggressive forms, circulating GDF-15 levels were assessed in two independent cohorts of EHE patients, one retrospective and one prospective. The results provided evidence of an association between circulating GDF-15 levels and the aggressiveness of EHE. In summary, these findings suggest that GDF-15 can serve as a biomarker for EHE aggressiveness and may have implications for monitoring the effectiveness of sirolimus in EHE patients.

2024-04-24 | GSE246235 | GEO

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