Disrupted mitochondrial function in aged human dermal fibroblasts
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ABSTRACT:
PROVIDER: PRJNA545351 | ENA |
REPOSITORIES: ENA
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Project description:Skin undergoes changes in structure and function with age, including a shift in metabolic programs. This is particularly evident relative to mitochondrial function in skin cells. Dermal fibroblasts have been known to accumulate damage caused by both external and internal stressors, leading to altered bioenergetics that limits efficient synthesis of ATP and NAD+. To better understand the changes in mitochondrial function with age, metabolic profiles and transcriptomic profiles of primary dermal fibroblasts from varying aged donors were analysed.
2020-10-26 | GSE131938 | GEO
Project description:Extrinsic skin ageing converges on the dermis, a post-mitotic tissue compartment consisting of extracellular matrix and long-lived fibroblasts prone to damage accumulation and maladaptation. Aged human fibroblasts exhibit mitochondrial and nuclear dysfunctions, but it is unclear whether these are cause or consequence of ageing. We report on a systematic study of human dermal fibroblasts retrieved from female donors aged 20-67 years and analyzed in primary culture at low population doubling precluding replicative senescence. Genome-wide array analysis failed to detect significant (>2-fold) age-related expression changes for individual genes, but gene set enrichment analysis revealed down regulation of many genes involved in mitochondrial metabolism and respiratory electron transport, extracellular matrix maintenance, cell cycle progression and protein translation. Consistent with these changes, mitochondrial content, respiratory function and cell proliferation declined with donor age. This was associated with inadequate nuclear mito-biogenesis, hypo- phosphorylation of AMP-dependent protein kinase alpha and upregulation of the alpha2-isoform, suggesting that inadequate mito-nuclear signalling could be the leading event entailing decreased expression of mitochondrial genes and compensatory down regulation of proliferation and protein synthesis. The comparatively few genes exhibiting age-associated up regulation were associate with cholesterol metabolism, immune reactions and mRNA processing, possibly also reflecting adaptation to inadequate mitochondrial function. Donors: 15 human female donors included in the study were aged 20, 21, 23, 26, 26, 40, 41, 42, 43, 49, 60, 62, 63, 64 and 67 years, thus covering the age spectrum 20 – 67 years and providing five biological replicates for each of the age groups “young” (20-30 years), “middle” (40-50 years) and “old” (60-70 years). Human dermal fibroblasts were isolated from skin specimen removed in the course of cosmetic surgery from the bottom side of female breast. Isolation and primary culture of the cells followed published procedures (Tigges and others 2013). Cells were not expanded beyond 12 population doublings, while replicative cell cycle arrest was determined to not occur before 40 population doublings.
2014-04-08 | E-GEOD-55118 | biostudies-arrayexpress
Project description:Primary human dermal fibroblasts were obtained from four young donors (ages 23–33) and five aged donors (ages 64–72) through the San Diego Nathan Shock Center (SD-NSC) Human Cell Models of Aging Core. Cells were cultured under standard conditions and subjected to bulk RNA sequencing to investigate age-associated transcriptional changes. Libraries were prepared using polyA selection and sequenced on the Illumina NovaSeq 6000 platform. Differential gene expression analysis was performed using the HOMER pipeline.
2026-03-02 | GSE307377 | GEO
Project description:Mouse primary dermal fibroblasts were treated with 100 nM endothelin-1 (ET1) synthetic peptide for 24 hours. Control samples received no ET1 peptide. The experiment compared treated to untreated to identify gene expression changes due to ET1 exposure. There are three biological replicates for both control and treated samples. These biological replicates represent separate derivations of primary dermal fibroblasts from genetically identical mouse litters aged 0-3 days.
2005-01-01 | E-MEXP-700 | biostudies-arrayexpress
Project description:scRNAseq of aging dermal fibroblasts
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Project description:The goal of this project is to compare the protein composition of the extracellular matrices (ECMs) deposited in vitro by wild type, heterozygous, or SPAG17 KO neonatal mouse dermal fibroblasts.
2022-09-22 | PXD019869 | Pride
Project description:Mouse primary dermal fibroblasts were treated with DNA demethylating agent 5-aza-2'-deoxycytidine. The exposure was 5um 5A2dC for 96 hours followed by recovery in normal medium for 24 hours. Three biological replicates were created for both the control and treated populations. Each biological replicate represents a separate derivation of dermal fibroblasts from genetically identical mouse pups aged 0-3 days. Cells reached passage 4 before initiating drug exposure.
2005-01-01 | E-MEXP-701 | biostudies-arrayexpress
Project description:Bulk RNA-seq analysis of primary human dermal fibroblasts from young and aged donors
| PRJNA1320544 | ENA
Project description:Extrinsic skin ageing converges on the dermis, a post-mitotic tissue compartment consisting of extracellular matrix and long-lived fibroblasts prone to damage accumulation and maladaptation. Aged human fibroblasts exhibit mitochondrial and nuclear dysfunctions, which may be a cause or consequence of ageing. We report on a systematic study of human dermal fibroblasts retrieved from female donors aged 20-67years and analysed ex vivo at low population doubling precluding replicative senescence. According to gene set enrichment analysis of genome wide array data, the most prominent age-associated change of the transcriptome was decreased expression of mitochondrial genes. Consistent with that, mitochondrial content and cell proliferation declined with donor age. This was associated with upregulation of AMP-dependent protein kinase (AMPK), increased mRNA levels of PPARγ-coactivator 1α (PGC1A) and decreased levels of NAD(+)-dependent deacetylase sirtuin 1. In the old cells the PGC1A-mediated mito-biogenetic response to direct AMPK-stimulation by AICAR was undiminished, while the PGC1A-independent mito-biogenetic response to starvation was attenuated and accompanied by increased ROS-production. In summary, these observations suggest an age-associated decline in PGC1A-independent mito-biogenesis, which is insufficiently compensated by upregulation of the AMPK/PGC1A-axis leading under baseline conditions to decreased mitochondrial content and reductive overload of residual respiratory capacity.
2014-04-08 | GSE55118 | GEO
Project description:Transcriptomic analysis of murine aging dermal fibroblasts at single cell level.
2018-11-14 | GSE111136 | GEO