An Improved Human 3D Skin Model for Aging Research
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ABSTRACT:
PROVIDER: PRJNA1238314 | ENA |
REPOSITORIES: ENA
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Project description:Current models used to study skin aging, including in vivo murine models, ex vivo human skin, and in vitro 2D cell cultures, present significant limitations in replicating the complexity of chronological human skin aging. To address this gap, we developed a novel 3D human full-thickness skin aging model using primary dermal fibroblasts and epidermal keratinocytes harvested from the same aged donors (average age 80 years). Comprehensive histological, immunostaining, and transcriptomic analyses of this aging model, compared to a young 3D skin model (average age 20 years), revealed distinct hallmarks of chronological skin aging, including reduced epidermal and dermal thickness, decreased extracellular matrix content, diminished cell proliferation, and increased cellular senescence. Furthermore, 3D aging skin model also showed reduced IGF-1 expression and induction of AP1/JunB, which were consistent with observations in aged human skin. Transcriptomic profiling further identified upregulated pathways associated with extracellular matrix degradation, cellular senescence, and immune responses, aligning closely with published data from human aged skin. This novel in vitro model faithfully recapitulates several key features of chronological skin aging, offering a robust platform for studying aging mechanisms and testing therapeutic interventions. We have used microarray to study the gene expression profile of 3D skin models
2025-03-31 | GSE292398 | GEO
Project description:Local IL-17 orchestrates skin aging
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Project description:We analyze the effect of magnetic 3D bioprinting using NanoShuttle-PL on the proteome of primary human skin fibroblasts and epidermal squamous cell carcinoma cells. NanoStuttle-PL employs magnetic nanoparticles that interact electrostatically with cells rendering them magnetic and allowing manipulation of their 3D assembly using external magnetic forces.
2021-07-16 | PXD023701 | Pride
Project description:Atopic dermatitis, a chronic inflammatory skin disease with increasing prevalance, is closely associated with skin barrier defects. A cytokine related to disease severity and inhibition of keratinocyte differentiation is IL-31. To identify its molecular targets, IL-31-dependent gene expression was determined in 3-dimensional organotypic skin models. In this data set we include expression data from human 3D skin models treated with or without IL-31 for 2, 8, 24 and 48 hours. As a source of keratinocytes HaCaT cells were used. These are immortalized primary keratinocytes. Human dermal fibroblasts were derived from a skin biopsy. A total of 8 samples were analyzed. We compared the control vs the IL-31 treated sample for each time point.
2016-02-29 | E-GEOD-76880 | biostudies-arrayexpress
Project description:This study examines differential gene expression in 3D skin organoids treated with Nintedanib.
2025-02-17 | GSE289407 | GEO
Project description:Human skin is composed of the cell-rich epidermis, the extracellular matrix (ECM) rich dermis, and the hypodermis. Within the dermis, a dense network of ECM proteins provides structural support to the skin and regulates a wide variety of signaling pathways which govern cell proliferation and other critical processes. Both intrinsic aging, which occurs steadily over time, and extrinsic aging (photoaging), which occurs as a result of external insults such as UV radiation, cause alterations to the dermal ECM. In this study, we utilized both quantitative and global proteomics, alongside single harmonic generation (SHG) and two-photon autofluorescence (TPAF) imaging, to assess changes in dermal composition during intrinsic and extrinsic aging. We find that both intrinsic and extrinsic aging result in significant decreases in structural ECM integrity, evidenced by decreasing collagen abundance and increasing fibril fragmentation, and ECM-supporting proteoglycans. Intrinsic aging also produces changes distinct from those produced by photoaging, including reductions in elastic fiber and crosslinking enzyme abundance. In contrast, photoaging is primarily defined by increases in elastic fiber-associated protein and pro-inflammatory proteases. Changes induced by photoaging are evident even in comparisons of young underarm and forearm skin, indicating that photoexposure experienced by an individual’s mid-20s is sufficient for large-scale proteomic alterations and that molecular-level changes due to photoaging are evident well before clinical indications are present. GO term enrichment revealed that both intrinsic aging and photoaging share common features of chronic inflammation.
2020-07-03 | PXD015982 | Pride
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:Organismal aging in mammals is manifested with architectural alteration and functional decline of multiple organs throughout the body. In aged skin, hairs are sparse, which has led to the hypothesis that the hair follicle stem cells (HFSCs) undergo epidermal differentiation during aging. Here, we employ single cell analysis to interrogate aging-related changes in the HFSCs. Unexpectedly, HFSCs maintain their lineage fidelity and show no signs of shifting to an epidermal fate. Despite maintaining lineage identity, HFSCs do show prevalent transcriptional changes in extracellular matrix genes. Of importance, these HFSC changes are accompanied by profound architectural perturbations in the aging stem cell niche. Upon surveying the dermis from young and aged skin, we also observe age-related changes in many non-epithelial cell types, including resident immune cells, sensory neurons, arrector pili muscles, and blood vessels – all of which have been previously associated with abilities to modulate hair follicle regeneration. Consistent with both intrinsic and extrinsic alterations in stem cell: niche communications, we find that in response to skin wounding, aged HFSCs repair the epidermis, but are defective in hair follicle regeneration. Intriguingly, whereas aged dermis cannot support young HFSCs, aged HFSCs can be rescued when supported by young dermis. Together, these findings favor a model where skin tissue microenvironment plays a dominant role in dictating the molecular properties and activities of HFSCs.
2019-12-31 | GSE124901 | GEO
Project description:3D Adipose Tissue Culture Links the Organotypic Microenvironment to Improved Adipogenesis
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Project description:Introduction: Sensitive skin is characterized by skin barrier disruption which is usually prone to react to external stimuli including UV, air pollution as well as cosmetic allergens. Sensitive skin tends to react with oxidative stress factors that could further lead to skin inflammation resulting in inflamm-aging. But almost no inflamm-aging models for sensitive skin, so it is worth constructing a method to screen anti-inflammaging ingredients and products. Methods: An in-vitro macrophages-fibroblasts model was established to evaluate the anti-inflammaging effect of ingredients. M1 phenotype and aging-associated gene expression were recorded by qPCR test to validate the inflamm-aging model. RNA sequencing was used to further elaborate the inflamm-aging mechanism of two validated ingredients. Results and conclusion: A novel in-vitro model of sensitive skin inflamm-aging was constructed by applying M1 phenotype of THP-1 culture medium supernatant to introduce the cellular senescence of the fibroblast cells, which could be used to screen out anti-inflammaging ingredients. In this model, supramolecular bakuchiol could promote collagen COL1A1 and COL3A3 production and inhibit inflammatory factors by increasing anti-inflammatory gene transcription (PTX3, ADAM33, and PDLIM1), while Terminalia chebula extract can inhibit cell senescence by reducing transcription of MAP4K2, and inflammatory factors CCL3 accumulation.
2025-04-16 | GSE286316 | GEO