Overexpression of HO-1 assisted PM2.5-induced apoptosis failure and autophagy-related cell necrosis

Zhou, Wei; Yuan, Xiaoyan; Zhang, Li; Su, Baoting; Tian, Dongdong; Yang, Li; Zhao, Jun; Wang, Yimei; Peng, Shuangqing

doi:10.1016/j.ecoenv.2017.07.047

Cited by 49 publications

(27 citation statements)

References 45 publications

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“…Many studies have demonstrated that Nrf2 signaling pathway played a key role in protection against stress, mainly via activation of multiple genes involved in antioxidant and detoxification pathways, including the phase II detoxification enzymes NQO1 and HO-1 [45,46]. Similarly, PM 2.5 has been demonstrated to elevate the expression of HO-1 and NQO1 in human lung epithelial cells (BEAS-2B) and human lung alveolar epithelial A549 cells [23,39]. Our results indicated that PM 2.5 -induced oxidative stress can lead to renal toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Overproduction of ROS induced by PM 2.5 exposure has been associated with cell homeostasis imbalance, mitochondrial damage and apoptosis [21,22]. Activation of apoptosis pathways, consisting of receptor-mediated (extrinsic) and mitochondrial (intrinsic) pathways, is a key step in apoptosis [23,24]. The death receptor pathway is characterized by TNF-α-induced apoptosis and recruitment of caspase family proteins including caspase-8 and caspase-3 [20].…”

Section: Introductionmentioning

confidence: 99%

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The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

et al. 2020

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Background: Exposure to airborne fine particulate matter (PM 2.5 ) has been reported to be harmful to the human kidney. However, whether the activation of oxidative stress and cell apoptosis plays key roles in the nephrotoxicity caused by PM 2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of cytotoxicity after PM 2.5 exposure in human proximal tubule epithelial cells (HK-2 cells).Results: PM 2.5 exposure resulted in a significant decrease in cell viability, with an increase in LDH release and the early kidney damage marker kidney injury molecule-1 (KIM-1) expression in a dose-dependent manner and timedependent manner. PM 2.5 exposure induced reactive oxygen species (ROS) generation and markedly elevated apoptosis in HK-2 cells. In addition, PM 2.5 exposure resulted in the activation of antioxidant pathway, as evidenced by the increased expressions of Nrf2, HO-1 and NQO1 and decreased expression of Keap1. Moreover, PM 2.5 exposure also induced the activation of apoptotic pathway, as evidenced by the increased expressions of pro-apoptotic proteins Bax, caspase-3 and caspase-8 and decreased expression of antiapoptotic protein Bcl-2. Conclusions:Our results demonstrated that both antioxidant pathway and apoptotic pathway played critical roles in the damage mediated by PM 2.5 in HK-2 cells. This study would give us a strategy to prevent the impairment of renal function by PM 2.5 induced through repression of oxidative stress and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

et al. 2020

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“…Cell apoptosis. Cell apoptosis was assessed by Annexin V-FITC/Propidium Iodide (PI) double staining using a cell apoptosis detection kit (Nanjing KeyGen Biotech Co., Ltd.) as previously described (16). After the indicated treatment, PIG1 and PIG3V cells were collected by centrifugation (500 x g for 5 min at 4˚C).…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analysis. A western blotting assay was performed to analyze the related protein expression, as previously described (16). Protein concentration was determined by a BCA assay (Beyotime Institute of Biotechnology).…”

Section: Determination Of Malondialdehyde (Mda) Superoxide Dismutasementioning

confidence: 99%

“…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). In a previous study, human lung epithelial cells (BEAS-2B) exposed to PM2.5 caused a high expression of heme oxygenase-1 (HO-1) and autophagy-related cell necrosis (16). While, hydrogen peroxide could induce oxidative stress in human melanocytes via nuclear factor erythroid 2-related factor 2 (Nrf2)-driven transcriptional activation of HO-1, and it could be a possible mechanism for melanocyte degeneration in vitiligo (17,18).…”

Section: Introductionmentioning

confidence: 99%

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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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Particulate matter 2.5 induced bronchial epithelial cell injury via activation of 5′‐adenosine monophosphate‐activated protein kinase‐mediated autophagy

Long

Jiang²,

et al. 2018

J of Cellular Biochemistry

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The impact of particulate matter 2.5 (PM2.5) on the respiratory system is a worldwide concern. However, the mechanisms by which PM2.5 causes disease are still unclear. In this study, we investigated the effect of PM2.5 on autophagy and studied the effect of PM2.5-induced autophagy and 5'-adenosine monophosphate-activated protein kinase (AMPK) on cell proliferation, cell cycle, apoptosis, reactive oxygen species (ROS), and airway inflammation using human bronchial epithelial cells 16HBE140 cells. Results showed that exposure of cells to PM2.5 at a concentration of 100 μg/mL for 24 hours was most effective for inhibiting cell viability. PM2.5 induced cell arrest in the G0/G1 phase and increased mitochondrial membrane potential, ROS, and cell apoptosis with increasing concentration. PM2.5 downregulated cyclin D and matrix metallopeptidase-9 (MMP-9) expression but upregulated tissue inhibitor of metalloproteinases-1 (TIMP-1) expression, significantly promoted interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) production, and enhanced the level and activation of AMPK. The levels of autophagy-related protein 5 (ATG5), Beclin-1, and LC3II/I were significantly increased by PM2.5. The activation of Unc-51-like autophagy activating kinase 1 was significantly inhibited by PM2.5. Moreover, ATG5 knockdown inhibited PM2.5-induced autophagy, ROS, and cell apoptosis significantly. The expression of cyclin D, MMP-9, and TIMP-1 was reversed by ATG5 suppression. PM2.5-induction of IL-6 and TNF-α was significantly inhibited by knockdown of ATG5. Thus, inhibition of autophagy protected the cells from PM2.5-induced injury. PM2.5 induced injury in human bronchial epithelial cells via activation of AMPK-mediated autophagy, suggesting possible therapeutic targets for the treatment of respiratory diseases.

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Overexpression of HO-1 assisted PM2.5-induced apoptosis failure and autophagy-related cell necrosis

Cited by 49 publications

References 45 publications

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

The activation of antioxidant and apoptosis pathways involved in damage of human proximal tubule epithelial cells by PM2.5 exposure

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

Particulate matter 2.5 induced bronchial epithelial cell injury via activation of 5′‐adenosine monophosphate‐activated protein kinase‐mediated autophagy

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