Expression data from whole human skin samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE134204 | GEO | 2020/07/31
REPOSITORIES: GEO
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Project description:Ageing compromises the mechanical properties of skin, with increased fragility and coincident slowing of the healing process making aged skin susceptible to chronic wounding. The ageing process is driven by an aggregation of damage to cells and extracellular matrix, compounded by regulatory changes, including age-associated hormonal dysregulation. Here we report on the correlation between mechanical properties and composition of skin from ovariectomised and chronologically aged mice, to assess the extent to which estrogen deprivation drives dermal ageing. We found that age and estrogen abrogation affected skin mechanical properties in contrasting ways: ageing lead to increased tensile strength and stiffness while estrogen deprivation had the opposite effect. Mass spectrometry proteomics showed that the quantity of extractable fibrillar collagen-I decreased with ageing, but no change was observed in ovariectomised mice. This observation, in combination with measurements of tensile strength, was interpreted to reflect changes to the extent of extracellular matrix crosslinking, supported by a significant increase in the staining of advanced glycation endpoints in aged skin. Loss of mechanical strength in the ovariectomy model was consistent with a loss of elastic fibres. Other changes in extracellular matrix composition broadly correlated between aged and ovariectomised mice, indicative of the role of estrogen-related pathways in ageing. This study offers a coherent picture of the relationship between tissue composition and mechanics, but suggests that the deleterious effects of intrinsic skin ageing are compounded by factors beyond hormonal dysregulation.
2019-03-11 | PXD012754 | Pride
Project description:Studies in model organisms suggest that aged cells can be functionally rejuvenated, but whether this concept applies to human skin is unclear. Here we apply deep sequencing of RNA 3' ends ("3-seq") to discover the gene expression program associated with human photoaging and intrinsic skin aging (collectively termed "skin aging") and the impact of broadband light (BBL) treatment. We find that skin aging was associated with the significantly altered expression level of 2,265 coding and noncoding RNAs, of which 1,293 became "rejuvenated" after BBL treatment, i.e. more similar in expression level of youthful skin. Rejuvenated genes (RGs) included several known key regulators of organismal longevity and their proximal long non-coding RNAs. Skin aging is not associated with systematic changes in 3' end mRNA processing. Hence, BBL treatment can restore the gene expression pattern of photoaged and intrinsically aged human skin to resemble young skin. In addition, our data reveals a novel set of targets that may lead to new insights into the human skin aging process. Examination of broadband light treated and untreated human skin transcriptomes of 5 women aged 50 years or more. They were compared to the skin transcriptomes of 5 young women aged 30 years or less.
2012-07-30 | E-GEOD-39170 | biostudies-arrayexpress
Project description:Ageing compromises the mechanical properties of skin, with increased fragility and coincident slowing of the healing process making aged skin susceptible to chronic wounding. The ageing process is driven by an aggregation of damage to cells and extracellular matrix, compounded by regulatory changes, including age-associated hormonal dysregulation. Here we report on the correlation between mechanical properties and composition of skin from ovariectomised and chronologically aged mice, to assess the extent to which estrogen deprivation drives dermal ageing. We found that age and estrogen abrogation affected skin mechanical properties in contrasting ways: ageing lead to increased tensile strength and stiffness while estrogen deprivation had the opposite effect. Mass spectrometry proteomics showed that the quantity of extractable fibrillar collagen-I decreased with ageing, but no change was observed in ovariectomised mice. This observation, in combination with measurements of tensile strength, was interpreted to reflect changes to the extent of extracellular matrix crosslinking, supported by a significant increase in the staining of advanced glycation endpoints in aged skin. Loss of mechanical strength in the ovariectomy model was consistent with a loss of elastic fibres. Other changes in extracellular matrix composition broadly correlated between aged and ovariectomised mice, indicative of the role of estrogen-related pathways in ageing. This study offers a coherent picture of the relationship between tissue composition and mechanics, but suggests that the deleterious effects of intrinsic skin ageing are compounded by factors beyond hormonal dysregulation.
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Project description:Profiling the skin microbiota composition from the face of healthy women. Exploring the differences between three age groups and between dry skin and not dry.
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Project description:Aging human skin undergoes significant morphological and functional changes such as wrinkle formation, reduced wound healing capacity, and altered epidermal barrier function. Besides known age-related alterations like DNA-methylation changes, metabolic adaptations have been more recently linked to impaired skin function in old humans. Understanding of these metabolic adaptations in aged skin are of special interest, because topical treatments could reverse age-dependent metabolic changes of human skin in vivo to affect age associated skin disorders. Results: We investigated the global metabolic adaptions in human skin during aging with a combined transcriptomic and metabolomic approach applied to epidermal tissue samples of young and old human volunteers. Our analysis confirmed known age-dependent metabolic alterations, e.g. reduction of coenzyme Q10 levels, and also revealed novel age effects that are seemingly important for skin maintenance. Integration of donor-matched transcriptome and metabolome data highlighted transcriptionally-driven alterations of metabolism during aging such as altered activity in upper glycolysis and glycerolipid biosynthesis or decreased protein and polyamine biosynthesis. Together, we identified several age-dependent metabolic alterations that might affect cellular signaling, epidermal barrier function, and skin structure and morphology. Conclusion: Our study provides a global resource on the metabolic adaptations and its transcriptional regulation during aging of human skin. Thus, it represents a first step towards an understanding of the impact of metabolism on impaired skin function in aged humans and therefore will potentially lead to improved treatments of age related skin disorders
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Project description:Skin aging is characterized by structural and functional changes that lead to slower wound healing and higher rate of infections, which contribute to age-associated frailty. This likely depends on synergy between alterations in the local microenvironment and stem cell–intrinsic changes, underscored by pro-inflammatory microenvironments that drive pleotropic changes. To date, little is known about the precise nature and origin of the proposed age-associated inflammatory cues, or how they affect different tissue resident cell types. Based on deep single-cell RNA-sequencing of the entire dermal compartment, we now provide a comprehensive understanding of the age-associated changes in all skin cell types. We show a previously unreported skew towards an IL-17–expressing phenotype of Th cells, γδ T cells and innate lymphoid cells in aged skin. Aberrant IL-17 signaling is common to many autoimmune (e.g., rheumatoid arthritis and psoriasis) and chronic inflammatory diseases. Importantly, in vivo blockade of IL-17–triggered signaling during the aging process reduces the pro-inflammatory state by affecting immune and non-immune skin cells of both dermis and epidermis. Strikingly, IL-17 neutralization significantly delays the appearance of age-related traits, such as decreased epidermal thickness, increased cornified layer thickness and ameliorated hair follicle stem cell activation and hair shaft regeneration. Our results indicate that the aged skin shows chronic and persistent signs of inflammation, and that age-associated increased IL-17 signaling could be targeted as a strategy to prevent age-associated skin ailments in elderly.
2022-12-31 | GSE193920 | GEO
Project description:The NRF2 transcription factor is a key regulator of the cellular antioxidant response, and pharmacological NRF2 activation is a promising strategy for the prevention of age-related diseases. Here we show, however, that genetic activation of Nrf2 in skin fibroblasts leads to the production of a matrisome, which is similar to aged skin and characterized by reduced synthesis and deposition of selected matrix proteins, including the major skin collagens. Mechanistically, the production of an aging matrisome results from Nrf2-mediated overexpression of microRNAs (miRs), which directly suppress collagen expression independently of myofibroblast differentiation. This is functionally important, as Nrf2 activation in fibroblasts caused structural abnormalities of the dermal ECM and increased the susceptibility to skin tearing, similar to aged skin. Activation of endogenous NRF2 was observed in human skin from elderly individuals in vitro and in vivo. These data implicate a key role for activated NRF2 in controlling age-related molecular and biomechanical skin alterations.
2022-09-20 | GSE180484 | GEO
Project description:Senescent cells accumulate in aging tissues, impairing their ability to undergo repair and regeneration following injury. Previous research has demonstrated that targeting tissue senescence with senolytics can enhance tissue regeneration and repair by selectively eliminating senescent cells in specific aged tissues. In this study, we focused on eliminating senescent skin cells in aged mice to assess the effects on subsequent wound healing. We applied ABT-263 (Navitoclax) and a DMSO control directly to the skin of 24-month-old mice over a 5-day period. Following ABT-263 treatment, aged skin showed decreased gene expression of senescent markers p16 and p21, accompanied by reductions in SA-β-gal and p21-positive cells compared to the DMSO-treated skin. However, ABT-263 treatment also triggered a temporary inflammatory response and macrophage infiltration in the skin. Bulk RNA sequencing of ABT-263-treated skin revealed prompt upregulation of genes associated with wound healing pathways, including hemostasis, inflammation, cell proliferation, angiogenesis, collagen synthesis, and extracellular matrix organization. Aged mice treated with ABT-263 exhibited accelerated wound closure compared to the DMSO control group. In conclusion, topical ABT-263 effectively reduced several senescence markers in aged skin, thereby priming the skin for improved subsequent wound healing. This enhancement may be attributed to ABT-263-induced senolysis and the resulting inflammation, which in turn stimulated the expression of genes involved in extracellular matrix remodeling and wound repair pathways.
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