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Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark (Human Myoblasts)

ABSTRACT: Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark (Human Myoblasts)

PROVIDER: PRJEB77671 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13366400.fastq.gz	Fastqsanger.gz
	ERR13366401.fastq.gz	Fastqsanger.gz
	ERR13366402.fastq.gz	Fastqsanger.gz
	ERR13366403.fastq.gz	Fastqsanger.gz
	ERR13366404.fastq.gz	Fastqsanger.gz

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Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark

Project description:Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark

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Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark (Murine Myotubes)

Project description:Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark (Murine Myotubes)

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Increased expression of Ectodysplasin A2 Receptor EDA2R is the most remarkable and ubiquitous aging-related transcriptional hallmark (Murine Myotubes)

Project description:We report that increased mRNA-expression of Ectodysplasin-A2-Receptor (EDA2R) is the most remarkable aging-associated transcriptional perturbation in humans and that its induction is confirmed in murine-models of Hutchinson-Gilford progeria syndrome and in other species. Up-regulation of EDA2R occurs in all solid-tissues and is complemented by the progressive transcriptional increase of its ligand in bloodstream. Strengthening of EDA2R/EDA-A2 signaling may exacerbate inflammation in ageing individuals which might be prevented by EDA2R/EDA-A2 blockade.

2024-09-13 | E-MTAB-14234 | biostudies-arrayexpress

Modulation of EDA2R/EDA-A2 signalling in Human Myoblasts

Project description:Transfection of human myoblasts was performed using Lipofectamine or electroporation. Skeletal muscle myoblasts isolated from a human male donor were transfected using the Lipofectamine™ 2000 Transfection Reagent (Invitrogen, 11668019). Twenty-four hours before transfections, cells were plated to a density of 17,500 cells/cm² in a 6-well plate. The transfection was performed according to the manufacturer’s protocol. For each well, 4 µg of plasmid DNA (EDA2R, Origene) and the appropriate amount of Lipofectamine™ 2000 were diluted in Opti-MEM™ I Reduced Serum Medium (Gibco, 31985070). After transfection, cells were incubated at 37 °C in a humidified atmosphere containing 5% CO₂ for 24 hours. For electroporation, skeletal muscle myoblasts isolated from a human male donor were transfected using the Amaxa™ Nucleofector Basic Kit for Primary Mammalian Smooth Muscle Cells (Lonza, VPI-1004). For each transfection condition, a total of 1 million cells were resuspended in the Nucleofector Solution provided with the kit. Then, 3 µg of plasmid DNA (EDA2R, Origene) was added to the cell suspension and subjected to nucleofection using the Amaxa Nucleofector Device with the A-033 program, as recommended by the manufacturer’s protocol. Following nucleofection, the cells were immediately transferred into pre-warmed complete growth medium and distributed into 3 wells of 9.6 cm² each. The cells were then incubated at 37 °C in a humidified atmosphere containing 5% CO₂ for 48 hours, until RNA extraction. For the ligand-based treatment, skeletal muscle myoblasts isolated from a human male donor were treated with EDA-A2 ligand (922-ED, R&D Systems) at the concentration of 250 ng/ml used in Bilgic et al., and incubated for an additional 48 hours, until RNA extraction.

2024-09-13 | E-MTAB-14239 | biostudies-arrayexpress

Increased ectodysplasin-A2-receptor EDA2R is a ubiquitous hallmark of aging and mediates parainflammatory responses.

Project description:Intensive efforts have been made to identify features that could serve as biomarkers of aging. Yet, drug-based interventions aimed at lessening the detrimental effects of getting older are lacking. This is largely attributable to tissue-specificity, sex-related differences, and to the difficulty of identifying actionable targets, which continues to pose a significant challenge. Here, we implement a bioinformatics approach revealing that aging-associated increase of the transmembrane Ectodysplasin-A2-Receptor is a prominent tissue-independent alteration occurring in humans and other species, and is particularly pronounced in models of accelerated aging. We show that strengthening of the Ectodysplasin-A2-Receptor signalling axis in myogenic precursors and differentiated myotubes suffices to trigger potent parainflammatory responses, mirroring aspects of aging-driven sarcopenia. Intriguingly, obesity, insulin-resistance, and aging-related comorbidities, such as type-2-diabetes, result in heightened levels of the Ectodysplasin-A2 ligand. Our findings suggest that targeting the Ectodysplasin-A2 surface receptor represents a promising pharmacological strategy to mitigate the development of aging-associated phenotypes.

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RNA-seq profiling of C/EBPβ-overexpressing myoblasts [proliferating myoblasts]

Project description:RNA-seq profiling of C/EBPβ-overexpressing myoblasts [proliferating myoblasts]

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RNA-seq profiling of C/EBPβ-overexpressing myoblasts [differentiating myoblasts]

Project description:RNA-seq profiling of C/EBPβ-overexpressing myoblasts [differentiating myoblasts]

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RNA-seq profiling of C/EBPβ-overexpressing myoblasts [proliferating myoblasts]

Project description:We previously identified C/EBPβ as an inhibitor of myogenic differentiation and a regulator of muscle satellite cell self-renewal. We found that C/EBPβ is regulated during the transition from proliferation to growth arrest in myoblasts and overexpression of C/EBPβ in myoblasts promotes cell growth arrest in vitro and improves engraftment of satellite cells into the stem cell niche in vivo. To identify the molecular mechanism by which C/EBPβ regulates myoblast proliferation and growth arrest, we performed RNA-seq on C/EBPβ-overexpressing myoblasts.

2020-12-18 | GSE152051 | GEO

SMCHD1 activates the expression of genes required for the expansion of human myoblasts (ChIP-seq)

Project description:In human muscle, SMCHD1 mutations are associated with the onset of FSHD2, but the mechanism driving the disease onset remains unclear. A commonly accepted explanation is the loss of SMCHD1 binding to the D4Z4 locus activates the expression of DUX4 in FSHD2 muscle. In this study, we used human myoblasts having DUX4 non-permissive 4qB alleles as a model to study DUX4-independent functions of SMCHD1 on myoblast cell growth. Surprisingly, depletion of SMCHD1 in these cells resulted in a cell proliferation defect. Despite the absence of DUX4 target genes’ activation, these cells showed a repression of PAX7 target genes (a hallmark of FSHD) and similar changes in expression profile compared to FSHD myoblasts. Interestingly, downregulation of cell proliferation-related genes and dysregulation of fibroblasts-specific genes were observed in SMCHD1 knockdown myoblasts and FSHD2 myoblasts but not FSHD1 myoblasts. Additionally, we identified LAP2 as direct targets of SMCHD1. Depletion of LAP2 leads to cell proliferation defect similar to the effect after SMCHD1 knockdown. These data imply that DUX4 is not the only driver for the onset of FSHD, and SMCHD1 has DUX4-independent functions in muscle growth and development.

2024-06-25 | GSE190829 | GEO

SMCHD1 activates the expression of genes required for the expansion of human myoblasts (RNA-seq)

2024-06-25 | GSE190828 | GEO