Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Quantitative analysis of skin proteomics in Chinese young and old populations by mass spectrometry

ABSTRACT: Aging is a normal physiological phenomenon of organisms. Skin aging is a specific manifestation of aging of local human organs. In this study, we used mass spectrometry to perform non-invasive analysis of the skin of 20 healthy young and elderly people in China. Quantitative proteomic analysis identified differentially expressed proteins.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Skin

SUBMITTER: MA JING

LAB HEAD: SEN YANG

PROVIDER: PXD018430 | Pride | 2020-08-05

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	19P0278001.raw	Raw
	19P0278002.raw	Raw
	19P0278003.raw	Raw
	19P0278004.raw	Raw
	19P0278005.raw	Raw

Items per page:

1 - 5 of 31

Publications

Quantitative proteomics analysis of young and elderly skin with DIA mass spectrometry reveals new skin aging-related proteins.

Ma Jing J Liu Mengting M Wang Yaochi Y Xin Cong C Zhang Hui H Chen Shirui S Zheng Xiaodong X Zhang Xuejun X Xiao Fengli F Yang Sen S

Aging 20200629 13

Skin aging is a specific manifestation of the physiological aging process that occurs in virtually all organisms. In this study, we used data independent acquisition mass spectrometry to perform a comparative analysis of protein expression in volar forearm skin samples from of 20 healthy young and elderly Chinese individuals. Our quantitative proteomic analysis identified a total of 95 differentially expressed proteins (DEPs) in aged skin compared to young skin. Enrichment analyses of these DEPs ...[more]

PMID: 32602849

Similar Datasets

Potential ATF6 regulatory proteins were screened by proteomics using pancreatic tissues of PRSS1 transgenic mice treated with caerulein

Project description:Humanized PRSS1 transgenic mice were constructed and treated with caerulein to mimic the development of human AP and CP. Potential ATF6 regulatory proteins in pancreatitis were screened by proteomics using pancreatic tissues of PRSS1 AP mice.

2021-09-09 | PXD016703 | Pride

Rad21-mediated NF-κB signaling limits hematopoietic stem cell self-renewal in aging and inflammation

Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.

2018-11-28 | PXD011537 | Pride

Glyoxal induces senescence of human keratinocytes through oxidative stress and activation of the AKT/FOXO3a/p27KIP1 pathway

Project description:Senescence is a well-known cellular event characterized by specific markers like a permanent cell proliferation arrest and the secretion of messenger molecules forming the Senescence-Associated Secretory Phenotype (SASP). The SASP composition depends on many factors such as the cell type or the nature of the stress that induced senescence. Since the skin constitutes a barrier with the external environment, it is particularly subjected to different types of stresses and thus to premature cellular aging. The dicarbonyl compounds glyoxal and methylglyoxal are precursors of Advanced Glycation End-products (AGEs), known to be a feature of normal and pathological aging. In this study, we have demonstrated that glyoxal provokes oxidative stress by increasing ROS and AGEs levels and can induce senescence in human keratinocytes. An “early-stage” senescence phenotype characterized by a cell cycle arrest mediated by the AKT-FOXO3-p27KIP1 pathway and a “late-stage” senescence maintained by the p16INK4/pRb pathway were evidenced. Moreover, we characterized the resulting secretory phenotype during early senesecence by mass spectrometry. Our study provides evidence that glyoxal can affect keratinocyte function and act as a driver of human skin aging. Hence, senotherapeutics aimed at modulating glyoxal-associated senescence phenotype could be relevant to prevent the aging process in skin.

2022-01-03 | PXD025184 | Pride

Reduced proteasome activity in the aging brain results in ribosome stoichiometry loss and aggregation

Project description:A progressive loss of protein homeostasis is characteristic of aging and a driver of neurodegeneration. To investigate this process quantitatively, we characterized proteome dynamics during brain aging in the short-lived vertebrate Nothobranchius furzeri combining transcriptomics and proteomics. We detected a progressive reduction in the correlation between protein and mRNA mainly due to post-transcriptional mechanisms that account for over 40% of the age-regulated proteins. These changes cause a progressive loss of stoichiometry in several protein complexes, including ribosomes, which show impaired assembly and are enriched in protein aggregates in old brains. Mechanistically, we show that reduction of proteasome activity is an early event during brain aging and is sufficient to induce proteomic signatures of aging and loss of stoichiometry in vivo. Using longitudinal transcriptomic data, we show that the magnitude of early life decline in proteasome levels is the major risk factor for mortality. Our work defines causative events in the aging process that can be targeted to prevent loss of protein homeostasis and delay the onset of age-related neurodegeneration.

2020-06-22 | PXD016459 | Pride

Hypoxia and Foxn1 alter dermal fibroblasts proteomics signature to redirect scar-less to scar-forming skin wound healing in Foxn1-/- mice

Project description:Hypoxia is one of the factors that govern reparative vs regenerative skin wound healing. Data-independent acquisition (DIA) experiment was carried out to study the effect of hypoxia and Foxn1 on mice dermal fibroblast proteomics signature and skin wound healing of Foxn1-deficient (Foxn1-/-) mice.

2024-06-20 | PXD041939 | Pride

Facial Skin Biophysical Multi-Parameter and Microbiome-Based Korean Skin Cutoype (KSC) Determination

Project description:In this study, we conducted an integrated analysis of skin measurements, clinical BSTI surveys, and the skin microbiome of 950 Korean subjects to examine the ideal skin microbiome-biophysical association. By utilizing four skin biophysical parameters, we identified four distinct Korean Skin Cutotypes (KSCs) and categorized the subjects into three aging groups based on their age distribution. We established strong connections between 15 core genera and the four KSC types within the three aging groups, revealing three prominent clusters of the facial skin microbiome. Together with skin microbiome variations, skin tone/elasticity distinguishes aging groups while oiliness/hydration distinguishes individual differences within aging groups. Our study provides prospective reality data for customized skin care based on the microbiome environment of each skin type.

| EGAS00001007334 | EGA

Single-Cell RNA Sequencing Reveals Age-Related Changes in Epidermal Cell Populations and Interactions

Project description:Utilizing single-cell RNA sequencing, we analyzed epidermal cells from young (20-30 years old) and elderly (60+ years old) subjects. Our findings reveal that aged epidermis exhibits increased expression of inflammation-related genes and pathways associated with nonsense-mediated decay, oxidative phosphorylation, and apoptotic signaling, predominantly in keratinocytes. Furthermore, we observed a reduction in cell-to-cell interactions from the proliferative basal and granular layers to other epidermal cells. This study underscores how epidermal aging primarily impacts keratinocytes and diminishes intercellular interactions, unveiling a novel mechanism of skin aging.

2024-11-15 | GSE281449 | GEO

Region-specific proteome changes of the intestinal epithelium during aging and dietary restriction

Project description:The small intestine is responsible for nutrient absorption and it is one of the most important interfaces between the environment and our body. During aging, changes in the structure of the epithelium lead to food malabsorption and reduced barrier function thus increasing disease risk in aging. The molecular drivers of these alterations remain poorly understood. Here, we compared the proteomes of small intestinal crypts from mice across different anatomical regions and age groups. We found that aging alters epithelial immune responses, metabolic networks and stem cell proliferation, and it is accompanied by a region-dependent skewing in the cellular composition of the intestinal epithelium. Of note, a short period of dietary restriction followed by re-feeding partially restores the epithelium to a youthful state by promoting the differentiation of intestinal stem cells (ISCs) towards the secretory lineage. Using in vitro and in vivo studies, we identify Hmgcs2 (3-hydroxy-3-methylglutaryl-CoA synthetase 2) – the rate limiting enzyme in the synthesis of ketone bodies – as a modulator of ISCs differentiation, which responds to dietary changes. This study provides an atlas of age-dependent proteome changes in defined regions of the intestinal epithelium and characterizes how young and old mice adapt to drastic changes of diet, such as dietary restriction and re-feeding.

2020-04-29 | PXD014311 | Pride

Histone deacetylase inhibition mitigates fibrosis-driven disease progression in recessive dystrophic epidermolysis bullosa

Project description:To delineate sodium valproate (VPA) molecular effects underlying mitigation of skin fibrosis in RDEB mice, mass spectrometry-based expression proteomics was performed on protein extracts from back skin of 16 weeks-old VPA-treated RDEB mice, vehicle-treated RDEB mice and WT littermates.

2024-08-31 | PXD047998 | Pride

Mapping sites of carboxymethyllysine modification on proteins reveals consequences for proteostasis and cell proliferation

Project description:Posttranslational mechanisms play a key role in modifying the abundance and function of cellular proteins. Among these, modification by advanced glycation end products (AGEs) has been shown to accumulate during aging and age-associated diseases but specific protein targets and functional consequences remain largely unexplored. Here, we devised a proteomic strategy to identify specific sites of carboxymethyllysine (CML) modification, one of the most abundant AGEs. We identified over 1000 sites of CML modification in mouse and primary human cells treated with the glycating agent glyoxal. By using quantitative proteomics, we found that protein glycation triggers a proteotoxic response and directly affects the protein degradation machinery. We show that glyoxal induces cell cycle perturbation of primary endothelial cells and that CML modification interferes with acetylation of tubulins and microtubule dynamics. Our data demonstrate the relevance of AGE modification for cellular function and pinpoints specific protein networks that might become compromised during aging.

2021-11-25 | PXD021891 | Pride