Endoplasmic reticulum stress aggravates copper-induced apoptosis via the PERK/ATF4/CHOP signaling pathway in duck renal tubular epithelial cells

Wang, Xiaoyu; Yu, Zhuang; Fang, Yukun; H, Cao; Zhang, Caiying; Xing, Chenghong; Guo, Xiaomin; Li, Guyue; Liu, Ping; Hu, Guoliang; Yang, Fan

doi:10.1016/j.envpol.2020.115981

Cited by 44 publications

(22 citation statements)

References 44 publications

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“…IRE1 and ATF‐6 are transferred into the nucleus and bind to the ER stress response element to initiate the transcription and expression of CHOP. The transcription factor ATF‐4 which is the downstream of PERK can bind to the AARE domain of the CHOP and promote CHOP expression, then down‐regulate the expression of anti‐apoptotic protein Bcl‐2 56,57 . In our experiment, the findings indicated that DLM exposure obviously induced ER stress and further triggered neuronal apoptosis in quail cerebrum.…”

Section: Discussionmentioning

confidence: 53%

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Han

et al. 2022

Environmental Toxicology

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Deltamethrin (DLM) is a widely used and highly effective insecticide. DLM exposure is harmful to animal and human. Quail, as a bird model, has been widely used in the field of toxicology. However, there is little information available in the literature about quail cerebrum damage caused by DLM. Here, we investigated the effect of DLM on quail cerebrum neurons. Four groups of healthy quails were assigned (10 quails in each group), respectively given 0, 15, 30, and 45 mg/kg DLM by gavage for 12 weeks. Through the measurements of quail cerebrum, it was found that DLM exposure induced obvious histological changes, oxidative stress, and neurons apoptosis. To further explore the possible molecular mechanisms, we performed real-time quantitative PCR to detect the expression of endoplasmic reticulum (ER) stressrelated mRNA such as glucose regulated protein 78 kD, activating transcription factor 6, inositol requiring enzyme, and protein kinase RNA (PKR)-like ER kinase. In addition, we detected ATP content in quail cerebrum to evaluate the functional status of mitochondria. The study showed that DLM exposure significantly increased the expression of ER stress-related mRNA and decreased ATP content in quail cerebrum tissues. These results suggest that chronic exposure to DLM induces apoptosis of quail cerebrum neurons via promoting ER stress and mitochondrial dysfunction. Furthermore, our results provide a novel explanation for DLM-induced apoptosis of avian cerebrum neurons.

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Section: Discussionmentioning

confidence: 53%

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Han

et al. 2022

Environmental Toxicology

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“…Curcumin has been reported to increase the expression of ATF4 and CHOP, which are considered the hallmarks of ER stress-induced apoptosis (49,50). During severe or prolonged ER stress, ATF4 is activated and binds to AARE1 on the CHOP promoter, further promoting the expression of the ER stress-associated apoptotic factor CHOP (51)(52)(53). After curcumin treatment, the expression levels of ATF4, and CHOP increased in ACC cells in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Curcumin induces apoptosis and inhibits the growth of adrenocortical carcinoma: Identification of potential candidate genes and pathways by transcriptome analysis

et al. 2021

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Adrenocortical carcinoma (ACC) is an endocrine tumour with high malignancy, high invasiveness and poor prognosis. Curcumin, a major component in turmeric, has been reported to have good efficacy and biological safety in treating cancer. However, the role and mechanism of curcumin in ACC have not yet been fully investigated and were thus the focus of this study. In vitro, ACC SW-13 and NCI-H295R cells were treated with curcumin and their viability, migration and invasion were assessed by CCK-8 and Transwell assays. Apoptosis was detected via flow cytometry and western blotting. High-throughput sequencing and comprehensive bioinformatics analyses were performed to elucidate the molecular processes underlying curcumin activity. In vivo, SW-13 cells were injected into nude mice, and the tumour volumes and weights were observed after 2 weeks of curcumin treatment. Organelle changes were observed by electron microscopy, and potential candidate genes and pathways were analysed by RT-qPCR and western blotting. The role of the C/EBP homologous protein (CHOP) target gene in curcumin-induced ACC cell apoptosis was verified via lentiviral transfection experiments. Curcumin inhibited the viability, migration and invasion, and induced the apoptosis of ACC cells. Transcriptome sequencing analysis showed that curcumin treatment markedly changed the gene expression levels. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses showed that the MAPK and endoplasmic reticulum (ER) stress pathways were the predominant pathways associated with curcumin-induced apoptosis of ACC cells. Subsequent in vivo and in vitro results demonstrated that the JNK, p38 MAPK and ER stress pathways were activated in curcumin-treated ACC cells, and that CHOP induction was responsible for curcumin-induced apoptosis of ACC cells. In summary, curcumin induced ACC cell apoptosis and inhibited tumour growth by activating the JNK, p38 MAPK and ER stress pathways. Thus, curcumin may be a potential therapeutic drug for ACC.

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“…On the other hand, appropriate endoplasmic reticulum stress promotes the survival of cells, and when long-term or severe endoplasmic reticulum stress occurs, the protective unfolded protein pathway fails to restore homeostasis, leading to endoplasmic reticulum dysfunction, and may initiate the apoptotic signal [11,59]. Past studies suggested that PERK could induce the expression of the pro-apoptotic transcription factor CHOP [60], thereby inhibiting the level of anti-apoptotic protein Bcl-2, and change the conformation of Bax and Bak to induce apoptosis [61,62]. Some researches have shown that the loss of CHOP can prevent cell apoptosis after persistent endoplasmic reticulum stress [63].…”

Section: Discussionmentioning

confidence: 99%

Zinc Alleviates Arsenic-Induced Inflammation and Apoptosis in the Head Kidney of Common Carp by Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress

Xing

Zhang

Chi

2021

Biol Trace Elem Res

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Arsenic (As) pollution is ubiquitous in water, which shows immunotoxicity to aquatic organisms. As an indispensable regulator of gene transcription and enzymatic modification, zinc (Zn) may play a preventive and therapeutic effect on As toxicity. The purpose of this study was to investigate the interactions of As and Zn on the head kidney of common carp Cyprinus carpio. Herein the carp were treated alone or in combination with waterborne As 3+ (2.83 mg/L) and/or Zn 2+ (1 mg/L). Results suggested a head kidney-toxic effect of As exposure, which was manifested by the histopathological damage of the head kidney, elevation of nuclear translocation of pro-inflammatory nuclear factor-kappa light chain enhancer of B cells (NF-κB), and blockage of the anti-oxidative nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. The global activation of three endoplasmic reticulum (ER) stress pathways led to the execution of programmed cell death, including ER apoptosis mediated by C/EBP-homologous protein (CHOP), death receptor-mediated exogenous cell apoptosis, and the endogenous apoptosis executed by Caspases9. The combined application of Zn can significantly improve the histopathological damage of the head kidney, the imbalance of the antioxidant system, and the apoptosis outcomes due to ER stress. In conclusion, this study indicates that Zn has an antagonistic effect on the head kidney injury of common carp induced by sub-chronic As exposure. The results of this study provide basic data for the risk assessment of As accumulation in an aquatic environment and a reference for the use of Zn preparation in aquaculture.

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Endoplasmic reticulum stress aggravates copper-induced apoptosis via the PERK/ATF4/CHOP signaling pathway in duck renal tubular epithelial cells

Cited by 44 publications

References 44 publications

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Curcumin induces apoptosis and inhibits the growth of adrenocortical carcinoma: Identification of potential candidate genes and pathways by transcriptome analysis

Zinc Alleviates Arsenic-Induced Inflammation and Apoptosis in the Head Kidney of Common Carp by Inhibiting Oxidative Stress and Endoplasmic Reticulum Stress

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