ScRNAseq of aging dermal fibroblasts
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA435994 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6783030_1.fastq.gz | Fastqsanger.gz | |||
| SRR6783030_2.fastq.gz | Fastqsanger.gz | |||
| SRR6783040_1.fastq.gz | Fastqsanger.gz | |||
| SRR6783040_2.fastq.gz | Fastqsanger.gz | |||
| SRR6783050_1.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptomic analysis of murine aging dermal fibroblasts at single cell level.
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Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
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Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
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Project description:To investigate aging heterogeneity in tissue-regeneration cells, we conducted RNA-seq analysis of human dermal fibroblasts (hDFs) at two distinct aging stages: passage 5 (p5) and passage 15 (p15). hDFs were cultured under standard conditions, and total RNA was extracted for sequencing. Transcriptomic profiling was performed to identify differentially expressed genes associated with cellular aging. This RNA-seq dataset was used to validate the phenotypic changes observed via a label-free, nondestructive single-cell analytics platform called nanosensor chemical cytometry (NCC). The integrated analysis revealed that transcriptomic aging signatures correspond with aging phenotypes such as changes in cell size, shape, refractive index, and H2O2 efflux. This dataset provides insight into the molecular mechanisms underlying cell aging and supports the development of predictive models for therapeutic performance in regenerative medicine.
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Project description:During aging, stromal functions are thought to be impaired, yet little is known whether this stems from molecular and cellular changes of fibroblasts, a major component of stroma. Using population- and single-cell whole transcriptomics, and long-term lineage tracing, we studied alterations in murine dermal fibroblasts during physiological aging under different dietary regimes known to affect longevity. We show that the identity of aged fibroblasts becomes undefined, with the distinct fibroblast states present in young skin no longer clearly demarcated. In addition, old fibroblasts not only reduce the expression of genes involved in the formation of the extracellular matrix, but intriguingly, also gain adipogenic traits, paradoxically becoming similar to neonatal pro-adipogenic fibroblasts. These age-related alterations are sensitive to systemic changes in metabolism: long-term caloric restriction prevents them in old fibroblasts in a reversible manner, whereas a high-fat diet potentiates them in young fibroblasts. Finally, inhibition of the master regulator of adipogenesis, PPARgamma, attenuates fibroblast aging in vivo, providing potential anti-aging therapeutic alternatives to caloric restriction.
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Project description:In this study, we have analyzed DNA methylation changes upon aging of human dermal fibroblasts by using the HumanMethylation27 BeadChip assessing 27,578 unique CpG sites. Cells were isolated from skin samples donated by young (6-23 years) and elderly (60-73 years) patients undergoing surgical interventions. Strikingly, global DNA-methylation profiles of fibroblasts from the same anatomical site clustered closely together indicating that fibroblasts maintain positional memory even after in vitro culture.
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