Particulate matter (PM)2.5 affects keratinocytes via endoplasmic reticulum (ER) stress-mediated suppression of apoptosis

Kim, J. H.; Son, Ji‐Won; Kim, J.; Kim, M. G.; Jeong, Soon-Wook; Park, T. J.; Son, Sang Wook; Ryu, Hwa Jung

doi:10.1007/s13273-019-00065-6

Cited by 11 publications

(8 citation statements)

References 25 publications

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“…The expression and the subsequent nuclear translocation of one of these transcription factors, namely the nuclear factor erythroid 2related factor 2 (Nrf2), is increased in vitro upon exposure to PM [127,138,145]. In turn, Nrf2 target genes and their protein expression such as heme oxygenase 1 (HMOX1), NAD(P) H quinone dehydrogenase 1 (NQO1), glutathione S-transferases (GSTs) are upregulated [127,133,138,141,143].…”

Section: Pm-induced Oxidative Stress Results In Lipid Protein and Dmentioning

confidence: 99%

“…Additionally, markers for proliferation, such as Ki67, 5-bromo-2′-deoxyuridine (BrdU) incorporation, and proliferating cell nuclear antigen (PCNA), were shown to be decreased upon PM exposure [125,130]. Reduced expression of differentiation and proliferation markers was also shown in 2D models, i.e., HaCaT and NHEK cells [122,125,127,140,141,143,144].…”

Section: Physical Barriermentioning

confidence: 98%

“…CYP enzymes can metabolize PAHs, and the formed metabolites can induce cell damage either by the formation of DNA, protein adducts, or the generation of ROS [195,[204][205][206][207][208]. Indeed, PM upregulates the CYP enzyme mRNA and protein expression in vitro and in vivo [119,128,129,134,135,139,141,167,171,172,178,187]. Other ROS producing enzymes are the members of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) family [209].…”

Section: Pm Triggers Exogenous and Endogenous Ros Formationmentioning

confidence: 99%

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Impact of airborne particulate matter on skin: a systematic review from epidemiology to in vitro studies

Dijkhoff¹,

Drašler²,

Karakoçak³

et al. 2020

Part Fibre Toxicol

126

116

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Background: Air pollution is killing close to 5 million people a year, and harming billions more. Air pollution levels remain extremely high in many parts of the world, and air pollution-associated premature deaths have been reported for urbanized areas, particularly linked to the presence of airborne nano-sized and ultrafine particles. Main text: To date, most of the research studies did focus on the adverse effects of air pollution on the human cardiovascular and respiratory systems. Although the skin is in direct contact with air pollutants, their damaging effects on the skin are still under investigation. Epidemiological data suggested a correlation between exposure to air pollutants and aggravation of symptoms of chronic immunological skin diseases. In this study, a systematic literature review was conducted to understand the current knowledge on the effects of airborne particulate matter on human skin. It aims at providing a deeper understanding of the interactions between air pollutants and skin to further assess their potential risks for human health. Conclusion: Particulate matter was shown to induce a skin barrier dysfunction and provoke the formation of reactive oxygen species through direct and indirect mechanisms, leading to oxidative stress and induced activation of the inflammatory cascade in human skin. Moreover, a positive correlation was reported between extrinsic aging and atopic eczema relative risk with increasing particulate matter exposure.

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Section: Pm-induced Oxidative Stress Results In Lipid Protein and Dmentioning

confidence: 99%

Section: Physical Barriermentioning

confidence: 98%

Section: Pm Triggers Exogenous and Endogenous Ros Formationmentioning

confidence: 99%

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Impact of airborne particulate matter on skin: a systematic review from epidemiology to in vitro studies

Dijkhoff¹,

Drašler²,

Karakoçak³

et al. 2020

Part Fibre Toxicol

126

116

View full text Add to dashboard Cite

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“…These data indicate that fisetin may be a potent bioactive compound against PM 2.5 -induced apoptosis in keratinocytes. On the contrary, high concentrations of PM 2.5 (1 mg/mL) inhibits ER stress and activates the inflammatory response in HaCaT keratinocytes [ 35 ], indicating that high concentrations of PM 2.5 give rise to ER stress-mediated chronic skin diseases. Nevertheless, further studies are necessary for investigating whether fisetin is able to protect against chronic skin diseases caused by high concentrations of PM 2.5 .…”

Section: Discussionmentioning

confidence: 99%

Fisetin Protects HaCaT Human Keratinocytes from Fine Particulate Matter (PM2.5)-Induced Oxidative Stress and Apoptosis by Inhibiting the Endoplasmic Reticulum Stress Response

et al. 2021

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Fine particulate matter (PM2.5) originates from the combustion of coal and is found in the exhaust of fumes of diesel vehicles. PM2.5 readily penetrates the skin via the aryl hydrocarbon receptor, causing skin senescence, inflammatory skin diseases, DNA damage, and carcinogenesis. In this study, we investigated whether fisetin, a bioactive flavonoid, prevents PM2.5-induced apoptosis in HaCaT human keratinocytes. The results demonstrated that fisetin significantly downregulated PM2.5-induced apoptosis at concentrations below 10 μM. Fisetin strongly inhibited the production of reactive oxygen species (ROS) and the expression of pro-apoptotic proteins. The PM2.5-induced apoptosis was associated with the induction of the endoplasmic reticulum (ER) stress response, mediated via the protein kinase R-like ER kinase (PERK)–eukaryotic initiation factor 2α (eIF2α)–activating transcription factor 4 (ATF4)–CCAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP) axis. Additionally, the cytosolic Ca2+ levels were markedly increased following exposure to PM2.5. However, fisetin inhibited the expression of ER stress-related proteins, including 78 kDa glucose-regulated protein (GRP78), phospho-eIF2α, ATF4, and CHOP, and reduced the cytosolic Ca2+ levels. These data suggest that fisetin inhibits PM2.5-induced apoptosis by inhibiting the ER stress response and production of ROS.

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“…Among diseases predicted by the molecular signaling networks, ‘dermatitis’, ‘psoriasis’, and several skin cancers have been shown to be important diseases in both the PM 10 and PM 2.5 associated genetic networks ( Fig. 1 ) [ 73 , 74 ].…”

Section: Comparison Of Pm 10 and Pm 25 In Terms Of Biological Pathway Alterationsmentioning

confidence: 99%

Genomic Approach to the Assessment of Adverse Effects of Particulate Matters on Skin Cancer and Other Disorders and Underlying Molecular Mechanisms

et al. 2021

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Air pollutants are in the spotlight because the human body can easily be exposed to them. Among air pollutants, the particulate matter (PM) represents one of the most serious toxicants that can enter the human body through various exposure routes. PMs have various adverse effects and classified as severe carcinogen by International Agency for Research on Cancer. Their physical and chemical characteristics are distinguished by their size. In this review, we summarized the published information on the physicochemical characteristics and adverse effects of PMs on the skin, including carcinogenicity. Through comparisons of biological networks constructed from relationships discussed in the previous scientific publications, we show it is possible to predict skin cancers and other disorders from particle-size-specific signaling alterations of PM-responsive genes. Our review not only helps to grasp the biological association between ambient PMs and skin diseases including cancer, but also provides new approaches to interpret chemical-gene-disease associations regarding the adverse effects of these heterogeneous particles.

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Particulate matter (PM)2.5 affects keratinocytes via endoplasmic reticulum (ER) stress-mediated suppression of apoptosis

Cited by 11 publications

References 25 publications

Impact of airborne particulate matter on skin: a systematic review from epidemiology to in vitro studies

Impact of airborne particulate matter on skin: a systematic review from epidemiology to in vitro studies

Fisetin Protects HaCaT Human Keratinocytes from Fine Particulate Matter (PM2.5)-Induced Oxidative Stress and Apoptosis by Inhibiting the Endoplasmic Reticulum Stress Response

Genomic Approach to the Assessment of Adverse Effects of Particulate Matters on Skin Cancer and Other Disorders and Underlying Molecular Mechanisms

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