Involvement of NLRP3/Caspase-1/GSDMD-Dependent pyroptosis in BPA-Induced apoptosis of human neuroblastoma cells

Wang, Congcong; Wang, Lei; Huang, Chengmeng; Liu, Yungang; Liu, Jian; Kuang, Hongxuan; Pang, Qihua; Han, Hongmei; Fan, Ruifang

doi:10.1016/j.bcp.2022.115042

Cited by 20 publications

(9 citation statements)

References 57 publications

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“…BPA has been found to induce NLRP3/Caspase-1-dependent pyroptosis in human neuroblastoma, osteoblasts, trachea and liver ( Wang et al, 2022 ; Zhang et al, 2022 ; Shi et al, 2023 ; Yin et al, 2023 ). Se deficiency treatment also induced NLRP3/Caspase-1-dependent pyroptosis in porcine spleen and chicken kidney ( Gu et al, 2022 ; Song et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Wu,

Su,

et al. 2024

Poultry Science

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Section: Discussionmentioning

confidence: 99%

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Wu,

Su,

et al. 2024

Poultry Science

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“…It is reported that oxidative stress has become a key factor in apoptosis induced by BPA exposure and Se deficiency. BPA exposure can promote oxidative stress and cause extensive apoptosis of human and animal tissues and cells, including mouse spermatocytes (C. Wang, Zhang, et al, 2017), chicken bursa cells (L. Liu et al, 2021), and human neuroblastoma cells (C. Wang, Wang, et al, 2022). Se deficiency or selenoprotein deficiency can induce apoptosis of human uterine smooth muscle cells (Y. Wang, Li, et al, 2022), chicken embryonic vascular smooth muscle cells (Q. Wang, Huang, et al, 2017), mouse neurons, and other cells by inducing oxidative stress (S. Z. Jia, Xu, et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A aggravate selenium deficiency‐induced apoptosis via miR‐215‐3p/Dio1 to activate ROS/PI3K/AKT pathway in chicken arterial

Fan

et al. 2023

Journal Cellular Physiology

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Both bisphenol A (BPA) and selenium (Se) deficiency can affect the expression of microRNAs (miRNAs), which can specifically regulate its target mRNA and induce apoptosis, and play a significant role in cardiovascular injury diseases. To explore the mechanism of apoptosis induced by BPA and Se deficiency in chicken arterial endothelial tissue and the role of miRNAs in this process, the model of BPA exposure/Se deficiency in chicken and PAEC cells have been employed. The targeting relationship between miR‐215‐3p and iodothyronine deiodinase 1 (Dio1) in PAEC was verified by double luciferase gene report. The level of miR‐215‐3p was detected by qRT‐PCR. The oxidative stress level of arterial endothelial cells was detected by oxidative stress kit and DCFH‐DA probe method. The PI3K/AKT pathway, mitochondrial dynamics, and apoptosis‐related genes were detected by qRT‐PCR and western blot. The mitochondrial ATP level and nitric oxide synthases (NOSs) level were detected with the kit. TUNEL, acridine orange/ethidium bromide, and flow cytometry were used to detect the level of apoptosis. The results showed that BPA exposure and Se deficiency led to overexpression of miR‐215‐3p, aggravated oxidative stress, inhibited activation of PI3K/AKT pathway, promoted mitochondrial division, increased expression of apoptosis related genes, and finally led to apoptosis of chicken arterial endothelial cells. We also established knockdown/overexpression models of miR‐215‐3p and Dio1 in vitro, and found that overexpression of miR‐215‐3p and knockout of Dio1 can induce apoptosis. Interestingly, miR‐215‐3p‐Inhibitor and N‐acetyl‐ l‐cysteine (NAC) partially prevented apoptosis caused by BPA exposure and Se deficiency, and LY294002 aggravated apoptosis. These results suggest that BPA exposure aggravates the apoptosis of Se deficient arterial endothelial cells in chickens by regulating the ROS/PI3K/AKT pathway activated by miR‐215‐3p/Dio1. The miR‐215‐3p/Dio1 axis provides a new way to understand the toxic mechanism of BPA exposure and Se deficiency, and reveals a new regulatory model of apoptosis damage in vascular diseases.

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“…This acts as the pyroptosis executor to release the N-terminal domain, which can cause membrane pores [ 41 ] to release intracellular contents, such as IL18, IL1β, and LDH, into the extracellular environment. This release will eventually lead to the occurrence of pyroptosis [ 42 ]. Activating transcription factor 4 ( ATF4 ) is an Endoplasmic Reticulum (ER) stress biomarker, the accumulation of which can activate JNK and retrain Akt phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

ESR1 dysfunction triggers neuroinflammation as a critical upstream causative factor of the Alzheimer’s disease process

Liu

Yuan

Niu

et al. 2022

Aging

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Alzheimer's disease (AD) accounts for approximately 60% of dementia cases worldwide. Advanced age is the most significant risk factor for AD and approximately two-thirds of cases relate to women. While the previous meta-analysis suggests that estrogen receptor (ESR) genetic polymorphisms are closely associated with dementia, the implications of this observation on a molecular level are not entirely understood. Our study explores this intricate molecular puzzle through the use of a variety of bioinformatics tools. Initially, we attempted to elucidate mechanisms underlying breast cancer development by identifying the high-throughput dataset of ESR1-knockdown breast cancer tissue samples. Surprisingly, KEGG pathway enrichment showed that the most frequently occurring proteins were related to axonal guidance and inflammation-related gene markers. These observations were supported by an external high throughput dataset of AD inflammatory samples in vivo. Our results suggest that ESR1 is modulated by apolipoprotein E (APOE) through CEBPB/ATF4, mir-155-5p, or mir-1-3p. Moreover, sea hare-hydrolysates (SHH), as one of the axonal guidance molecules, could regulate the STAT3/PRDM1/CEBPB pathway and consequently induce cell death through pyroptosis signaling pathways, trigger the secretion of IL1β, leading to neuroinflammation and worsening AD pathogenesis. Molecular docking verification demonstrated that the predicted natural products scoulerine and genistein displayed strong binding affinities for BACE1 and ESR1, respectively. This strategy can be used to design novel, personalized therapeutic approaches to treatment and a first-in-class clinical lead for the personalised treatment of AD.

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Involvement of NLRP3/Caspase-1/GSDMD-Dependent pyroptosis in BPA-Induced apoptosis of human neuroblastoma cells

Cited by 20 publications

References 57 publications

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Bisphenol A and selenium deficiency exposure induces pyroptosis and myogenic differentiation disorder in chicken muscle stomach

Bisphenol A aggravate selenium deficiency‐induced apoptosis via miR‐215‐3p/Dio1 to activate ROS/PI3K/AKT pathway in chicken arterial

ESR1 dysfunction triggers neuroinflammation as a critical upstream causative factor of the Alzheimer’s disease process

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