RNAseq of Normal Human Epidermal Keratinocytes (NHEKs) in UVB-induced senescence (UVB-SIPS, at 3 days or 5 days) or in replicative-like senescence (RS)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Emilie Bauwens
PROVIDER: E-MTAB-10969 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:RNAseq of Normal Human Epidermal Keratinocytes (NHEKs) in UVB-induced senescence (UVB-SIPS, at 3 days or 5 days) or in replicative-like senescence (RS)
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Project description:Cells experience oxidative stress and widespread cellular damage during stress-induced premature senescence (SIPS). Senescent cells show an increase in lysosomal content, which may contribute to mitigating cellular damage by promoting autophagy. This study investigates the dynamics of lysosomal quality control in human dermal fibroblasts (HDF), specifically examining lysosomal signaling pathways during oxidative stress-induced SIPS. Our results reveal distinct signaling responses between the initial stress phase and the ensuing senescent phenotype. During the stress phase, treatment with tBHP, which undermines the antioxidant response, leads to elevated reactive oxygen species (ROS) and lysosomal damage. ROS accumulation activates AMP-activated protein kinase (AMPK) and inhibits Akt, which correlates with the suppression of mammalian target of rapamycin (mTOR). Inactivation of mTOR during this phase aligns with the activation of transcription factor EB (TFEB), a key regulator of autophagy and lysosomal biogenesis. TFEB knockdown under stress increased apoptosis, highlighting the protective role of TFEB in the stress response. As cells transition to senescence, TFEB activity, required for the autophagic damage repair, becomes less critical. The decrease in ROS levels leads to the normalization of AMPK and Akt signaling, accompanied by the reactivation of mTOR. This reactivation of mTOR, which is critical for establishing the senescent state, is observed alongside the inactivation of TFEB. Consequently, as damage decreases, TFEB activity decreases. Our results suggest a dynamic interplay between TFEB and mTOR, highlighting a critical role of TFEB in ensuring cellular survival during SIPS induction but becoming dispensable once senescence is established.
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Project description:Although senescence has long been implicated in aging-associated pathologies, it is not clearly understood how senescent cells are linked to these diseases. To address this knowledge gap, we profiled cellular senescence phenotypes and mRNA expression patterns during replicative senescence in human diploid fibroblasts. We identified a sequential order of gain-of-senescence phenotypes: low levels of reactive oxygen species, cell mass/size increases with delayed cell growth, high levels of reactive oxygen species with increases in senescence-associated M-NM-2-galactosidase activity (SA-M-NM-2-gal), and high levels of SA-M-NM-2-gal activity. Gene expression profiling revealed four distinct modules in which genes were prominently expressed at certain stages of senescence, allowing us to divide the process into four stages: early, middle, advanced, and very advanced. Interestingly, the gene expression modules governing each stage supported the development of the associated senescence phenotypes. Senescence-associated secretory phenotype-related genes also displayed a stage-specific expression pattern with three unique features during senescence: differential expression of interleukin isoforms, differential expression of interleukins and their receptors, and differential expression of matrix metalloproteinases and their inhibitory proteins. The analysis of time series gene expression level during replicaive senescence.
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Project description:This study comprehensively investigates the photoprotective effects of aloin against UVB-induced damage in HaCaT cells, elucidating its antioxidant capacity and its role in preventing cellular apoptosis. The proteomic effect of 50 μg/mL aloin on HaCaT cell damage induced by UVB was evaluated through comparative protein expression. Compared to control cells, UVB irradiation significantly altered protein expression in HaCaT cells, with 64 proteins upregulated and 236 proteins downregulated. In cells treated with both UVB and aloin, 79 proteins were upregulated and 84 proteins were downregulated compared to the UVB-only group. Proteomic analysis showed that aloin modulated the expression of proteins involved in critical signaling pathways, including PI3K-Akt, p53, TGF-β and pathways in cancer, promoting cell survival. Aloin upregulated proteins associated with cell cycle regula-tion and antioxidant responses, such as CCND3, GSTM4, GNA12, SKIL, YWHAZ, and PKN3 while downregulating pro-apoptotic protein FOXO3.
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Project description:Betaine (trimethylglycine) is a non-toxic, highly water-soluble organic osmolyte widely used in skin care due to its assumed moisturizing and protective properties, but only few studies have addressed its specific effects in skin. Here, the cellular and molecular targets of betaine were analyzed by genome-wide expression analysis in organotypic cultures of rat epidermal keratinocytes (REK). In this model, we also examined whether betaine modifies the impacts of acute UVB exposure. The expression of several genes relevant to epidermal biology, proliferation/differentiation or malignancy as well as solute transport were verified by independent methods (qRT-PCR, western blotting). The data concerning changes in calcium metabolism after UVB exposure has been published separately (Bart et al., Br. J. Dermatol. 171:376-387, 2014). Organotypic cultures of rat epidermal keratinocytes (REK) were prepared by plating cells on a collagen-coated insert (submerged in medium), lifting the confluent cell layer to the air-liquid interface 3 days after plating. These 3D cultures were divided in four treatment groups with three replicates in each: control, betaine (10 mM), UVB (30 mJ/cm2) and betaine + UVB. Betaine was added to the cultures for 11 days, starting from day 4 until sample collection. UVB exposure was performed 24 h prior to sample collection for 2-week-old 3D cultures with a well-formed epidermal layer. For further details on the experimental set-up and characteristics of the UV source, please refer to Bart et al. (Br. J. Dermatol. 171:376-387, 2014) and Rauhala et al. (J. Biol. Chem. 288:17999-18012, 2013).
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