Analysis of PM 2.5 -induced cytotoxicity in human HaCaT cells based on a microfluidic system

Zhang, Yuxiao; Zheng, Lulu; Jiang, Tuo; Liu, Qi; Zhang, Xinlian; Xu, Zhixuan; Liu, Sixiu; Sui, Guodong

doi:10.1016/j.tiv.2017.04.018

Cited by 42 publications

(32 citation statements)

References 42 publications

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“…Based on the above evidence, we concluded that PM2.5-induced IL-1β production in oAβ-stimulated microglia was possibly dependent on NLRP3 inflammasome activation. This finding was in accordance with the previous studies conducted in human airway epithelial cells, macrophage, ventricular myocytes, and a human keratinocyte cell line [ 17 , 29 – 31 ]. However, gene knockout experiments have not been performed in the present study.…”

Section: Discussionsupporting

confidence: 94%

“…Then, we showed that PM2.5 exposure increased IL-1β production in oAβ-stimulated microglia. The result was supported by previous studies showing that PM2.5 caused IL-1β production in other cells, such as human airway epithelial cells, macrophage, ventricular myocytes, and a human keratinocyte cell line [ 17 , 29 – 31 ]. More importantly, the effects of PM2.5 on the neuronal injury were mitigated by IL-1ra, as IL-1ra decreased neuronal apoptosis in flow cytometry and increased neuronal viability in MTT assay.…”

Section: Discussionsupporting

confidence: 85%

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PM2.5 exposure aggravates oligomeric amyloid beta-induced neuronal injury and promotes NLRP3 inflammasome activation in an in vitro model of Alzheimer’s disease

Wang

Shi

et al. 2018

J Neuroinflammation

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BackgroundNumerous studies suggested that PM2.5 exposure was associated with increased risk of Alzheimer’s disease (AD). But the precise mechanisms by which PM2.5 contributed to AD pathogenesis have not been clarified.MethodsIn the presence or absence of neurons, oligomeric amyloid beta (oAβ)-primed microglia were stimulated with PM2.5. Firstly, we determined the effects of PM2.5 exposure on neuronal injury and inflammation in neurons-microglia co-cultures. Then, we examined whether NLRP3 inflammasome activation was involved in PM2.5-induced inflammation. After that, we investigated whether PM2.5 exposure increased ROS level in oAβ-stimulated microglia. At last, we examined whether ROS and NLRP3 inflammasome activation was required for PM2.5-induced neuronal injury in neurons-microglia co-cultures.ResultsIn the present study, we showed that PM2.5 exposure aggravated oAβ-induced neuronal injury and inflammation in neurons-microglia co-cultures via increasing IL-1β production. Further, PM2.5-induced IL-1β production in oAβ-stimulated microglia was possibly dependent on NLRP3 inflammasome activation. Meanwhile, PM2.5 exposure increased ROS level in oAβ-stimulated microglia. ROS was required for PM2.5-induced IL-1β production and NLRP3 inflammasome activation in oAβ-stimulated microglia. More importantly, ROS and NLRP3 inflammasome activation was required for PM2.5-induced neuronal injury in neurons-microglia co-cultures.ConclusionsFor the first time, these results suggested that the effects of PM2.5 under AD context were possibly mediated by NLRP3 inflammasome activation, which was triggered by ROS. Taken together, these findings have deepened our understanding on the role of PM2.5 in AD pathogenesis.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 85%

PM2.5 exposure aggravates oligomeric amyloid beta-induced neuronal injury and promotes NLRP3 inflammasome activation in an in vitro model of Alzheimer’s disease

Wang

Shi

et al. 2018

J Neuroinflammation

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“…In addition, a previous study identified that PM2.5 was a crucial risk factor for skin diseases and skin aging (11). The cytotoxicity of PM2.5 on human keratinocytes (HaCaT cells), which is related to the inflammatory response, could be a cause of PM2.5-induced skin injury (12). The main pathways of the PM2.5 toxic effect are related to oxidative stress injury, the inflammatory response, skin barrier function impairment and genetic damage (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

et al. 2020

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Recent growing evidence suggested that particulate matter 2.5 (PM2.5) has strong toxic effects on skin systems. However, the possible effects and the mechanisms of PM2.5 on vitiligo remain poorly understood. Therefore, the present study aimed to further investigate the effects and possible mechanisms of PM2.5 on vitiligo. Human keratinocytes (HaCaT cells) and human melanocytes (PIG1 cells and PIG3V cells) were exposed to PM2.5 (0-200 µg/ml) for 24 h. The cell viability of the three cell lines was measured by a Cell Counting Kit-8 assay. The secretions of stem cell factor (SCF) and basic fibroblast growth factor (bFGF) in HaCaT cells were evaluated by ELISA. The melanin contents, cellular tyrosinase activity, apoptosis, cell migration, malondialdehyde (MDA) contents, superoxide dismutase (SOD) levels, glutathione peroxidase (GSH-Px) levels and related protein expressions in PIG1 cells and PIG3V cells were evaluated by a NaOH assay, DOPA assay, Annexin V-FITC/Propidium Iodide staining, MDA assay, SOD assay, GSH-Px assay and western blotting, respectively. It was demonstrated that PM2.5 exposure inhibited cell viability of all three cell lines (HaCaT, PIG1 and PIG3V cells). PM2.5 exposure attenuated the secretions of SCF and bFGF in HaCaT cells. Moreover, PM2.5 exposure attenuated the activation of tyrosinase and melanogenesis, inhibited cell migration, and induced apoptosis and oxidative stress injury in PIG1 cells and PIG3V cells. In addition, PM2.5 exposure caused upregulated cytosolic cytochrome C and activated caspase-3 in PIG1 cells and PIG3V cells. Furthermore, PM2.5 exposure activated the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 signaling pathway. The present results suggested that PM2.5 exposure could inhibit the secretions of SCF and bFGF in keratinocytes, and cause oxidative stress injury and melanin metabolic disorder in melanocytes. Therefore, PM2.5 could be a new risk factor for vitiligo. PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

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“…Such cell lines can be keratinocyte cell lines, such as HaCaT or NHEK [47][48][49], or fibroblast cell lines, such as normal human foreskin-derived dermal fibroblasts (NHDF) [50,51]. These cells can be formed in a single layer or as a reconstructed skin model to create a more differentiated and accurate model of human skin characterized inner alia in the presence of the stratum corneum [40].…”

Section: In Vitro Efficacy Testingmentioning

confidence: 99%

“…Microfluidic devices, integrated with a cell culture with a protein microarray chip allows for a fast and reliable evaluation of the cell cytotoxicity and apoptosis in response to pollution [49].…”

Section: In Vitro Efficacy Testingmentioning

confidence: 99%

The Impact of Pollution on Skin and Proper Efficacy Testing for Anti-Pollution Claims

et al. 2018

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Exposure to pollution can cause oxidative stress, premature ageing, inflammation, and diseases. Since most of us are exposed to pollution, protection is important. This can be achieved through skin protection or through protection with respect to food and food supplements. There is a wide range of products on the market with anti-pollution claims. However, it is important that these claims are thoroughly validated by proper efficacy testing. When skin cells are exposed to pollution factors, changes in a number of skin properties can be observed, such as lipid composition, lipid and protein oxidation, pH, sebum secretion rate, oxidative stress, inflammation markers, and collagen and elastin levels. These can be measured and used as markers to verify anti-pollution claims. In the present review, we summarize some of the most important in vitro and in vivo tests that are used to determine if an ingredient or formulation has anti-pollution efficacy.

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Analysis of PM 2.5 -induced cytotoxicity in human HaCaT cells based on a microfluidic system

Cited by 42 publications

References 42 publications

PM2.5 exposure aggravates oligomeric amyloid beta-induced neuronal injury and promotes NLRP3 inflammasome activation in an in vitro model of Alzheimer’s disease

PM2.5 exposure aggravates oligomeric amyloid beta-induced neuronal injury and promotes NLRP3 inflammasome activation in an in vitro model of Alzheimer’s disease

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

The Impact of Pollution on Skin and Proper Efficacy Testing for Anti-Pollution Claims

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