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Comparative Analysis of Oral and Skin Keratinocytes Responses to Oxidative Stress

ABSTRACT: Oxidative stress caused by excessive reactive oxygen species (ROS) disrupts skin and oral epithelial homeostasis and contributes to skin aging, inflammation, periodontitis, and mucosal injury. As the principal defenders in both tissues, keratinocytes may exhibit divergent responses to oxidative stress. However, most existing studies have examined skin or oral keratinocytes in isolation, with few comparative investigations of their tolerance, repair capacity, and antioxidant mechanisms under oxidative stress. In this study, we systematically compared immortalized oral keratinocytes (TIGK) and skin keratinocytes (HaCaT) under hydrogen peroxide (H₂O₂)–induced oxidative stress. Functional analyses, including cell survival, ROS accumulation, wound healing, and proliferation recovery assays, were combined with transcriptomic profiling to evaluate differences in antioxidant and pro-oxidant systems. TIGK exhibited significantly higher survival rates, lower ROS accumulation, and superior migratory and proliferative recovery compared with HaCaT after oxidative insult. Transcriptomic analysis further revealed that TIGK consistently expressed higher levels of antioxidant genes and enzymes. In contrast, HaCaT showed greater ROS accumulation and relatively limited antioxidant defenses. Oral and skin keratinocytes adopt distinct adaptive mechanisms under oxidative stress. The intrinsic redox advantage of oral keratinocytes provides new insights into their rapid wound-healing capacity and may inform strategies to enhance epithelial resilience.

ORGANISM(S): Homo sapiens

PROVIDER: GSE308958 | GEO | 2026/03/12

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE308958_H2O2vsCtrl.HaCaT.Cutoff1_DEGs.csv.gz	Csv
	GSE308958_H2O2vsCtrl.TIGK.Cutoff1_DEGs.csv.gz	Csv
	GSE308958_HvsT.H2O2.Cutoff1_DEGs.csv.gz	Csv
	GSE308958_HvsT.Untreated.Cutoff1_DEGs.csv.gz	Csv

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Project description:Investigation of gene expression in cultured human skin epithelial keratinocytes (HaCaT) following non-thermal plasma treatment for 60 s, compared to untreated control. Non-thermal atmospheric pressure plasma has recently gained attention in the field of biomedical and clinical applications. In the area of plasma medicine research one promising approach is to promote wound healing by stimulation of cells involved. To understand basic molecular and cellular mechanisms triggered by plasma treatment we investigated biological effects of an argon plasma jet (kinpen) on human epithelial skin cells. Consequently, whole-genome microarrays were used to analyze this interaction in detail and identified a statistically significant modification of 3,274 genes including 1,828 up- and 1,446 down-regulated genes. Particularly, plasma-treated cells are characterized by differential expression of a considerable number of genes involved in the response to stress. In this regard, we found a plasma-dependent regulation of oxidative stress answer and increased expression of enzymes of the antioxidative defense system (e.g. 91 oxidoreductases). Our results demonstrate that plasma induces cell reactions of stress-sensing but also of proliferative nature. Consistent with gene expression changes as well as Ingenuity Pathway Analysis prediction, we propose that stimulating doses of plasma may protect epithelial skin cells in wound healing by promoting proliferation and differentiation. In conclusion, gene expression profiling may become an important tool in identifying plasma-related changes of gene expression. Our results underline the enormous clinical potential of plasma as a biomedical tool for stimulation of epithelial skin cells We investigated biological effects of an argon plasma jet on HaCaTs. Microarray were used to analyzed this interaction in detail. The transcripts analyzed in this study are further described in Schmidt et al. (2013): Non-thermal plasma treatment is associated with changes in transcriptome of human epithelial skin cells. Accepted in Journal Free Radical Research A study using total RNA recovered from at least 8 non-thermal plasma treated samples (300 ms*M-BM-5l/cell) and untreated HaCaT controls.

Project description:Solar ultraviolet (UV) radiation includes UVB (290-320 nm) and UVA (320-400 nm) wavelengths. While UVA is less energetic than UVB, it causes significant damage to both dermal and epidermal layers through acute and chronic exposure, leading to the accumulation of misfolded proteins and triggering endoplasmic reticulum (ER) stress. Mild exposure may activate a protective unfolded protein response, but prolonged exposure can result in cellular apoptosis. UVA radiation induces ER stress primarily through reactive oxygen species (ROS) production, activating downstream signaling pathways. Thus, identifying compounds that alleviate UVA-induced ER stress is crucial. Coreopsis tinctoria (CT), a traditional remedy from Xinjiang, China, contains bioactive compounds like flavonoids and polysaccharides, known for their antioxidant and anti-inflammatory effects.This study aims to evaluate the effectiveness of CT extract in reducing UVA-induced skin photodamage in human keratinocytes (HaCaT) by alleviating ER stress and apoptosis.We conducted transcriptomics analysis on UVA-exposed HaCaT cells, with and without CT extract treatment. Gene Ontology (GO) enrichment analysis highlighted differentially expressed genes associated with the ‘response to ER stress’ and ‘cellular response to misfolded proteins’ in the CT-treated cells compared to untreated UVA-irradiated cells. Western blotting, RT-qPCR, and immunofluorescence confirmed that markers related to ER stress, such as CHOP, pIRE1, and ATF6, were significantly downregulated following CT treatment. Additionally, apoptosis-related markers, including BCL2, cleaved-caspase 3, and cleaved-caspase 9, were reduced, and apoptosis assays using flow cytometry corroborated these findings. Notably, the application of tunicamycin, an ER stress inducer, negated the protective effects of CT against UVA-induced apoptosis and inflammation. Meanwhile, we identified the crosstalk pathway of Nrf2/HO-1 and ER stress by CT in eliciting the downstream antioxidant and detoxification targets. Furthermore, high-performance liquid chromatography (HPLC) analysis identified marein as the active compound responsible for the observed alleviation of ER stress following UVA exposure.These findings suggest that CT may serve as a promising therapeutic agent for protecting human keratinocytes from UVA-induced damage by mitigating ER stress and apoptosis.

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Comparative Analysis of Oral and Skin Keratinocytes Responses to Oxidative Stress

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