Cadmium-induced endoplasmic reticulum stress in chicken neutrophils is alleviated by selenium

Chen, Jianqiao; Pan, Tingru; Wan, Na; Sun, Zhepeng; Zhang, Ziwei; Li, Shu

doi:10.1016/j.jinorgbio.2017.02.022

Cited by 41 publications

(26 citation statements)

References 39 publications

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“…Although the cytotoxicity of Se is observed in the group treated with 7 ng/mL Se (sodium selenite), whether the same dose of organic Se, such as selenomethionine or selenised yeast, has a cytotoxic effect on mouse granulosa cells remains unclear and needs further investigation. Furthermore, Se also has been documented to decrease the apoptosis of immune cells by suppressing ER stress in chickens [19]. The CHOP/ caspase-3 apoptotic signaling pathway has been implicated in the inhibitive effects of Se on lead-induced apoptosis via ER stress pathway in chicken testes [37], indicating that ER stress-mediated apoptosis pathway plays an important role in the protective effects of selenium against apoptosis induced by different pathological factors.…”

Section: Discussionmentioning

confidence: 99%

“…Glucose-regulated protein 78 CHOP CCAAT/enhancer-binding protein (C/EBP) homologous protein CYP19A1 Cytochrome P450 family 19…”

Section: Hsmentioning

confidence: 99%

“…Because of its well-known function as an antioxidant, Se has been widely used for regulating the metabolic disorders and reproductive physiological functions [18]. Se has been documented to effectively protect certain cells against the toxicant and ER stress induced apoptosis [19]. Nevertheless, it is still not fully understood whether Se has a protective effect through the inhibition of ER stress signaling against heat stress-induced apoptosis in mouse granulosa cells.The aim of this study was to explore the effects of Se on chronic heat stress-induced damage in granulosa cells using an in vitro mouse granulosa cell model, and to evaluate the potential mechanism by which Se attenuates cell apoptosis.…”

mentioning

confidence: 99%

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Selenium Attenuates Chronic Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in Mouse Granulosa Cells

et al. 2020

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Heat stress induces apoptosis in various cells. Selenium, an essential micronutrient, has beneficial effects in maintaining the cellular physiological functions. However, its potential protective action against chronic heat stress (CHS)-induced apoptosis in granulosa cells and the related molecular mechanisms are not fully elucidated. In this study, we investigated the roles of selenium in CHS-induced apoptosis in mouse granulosa cells and explored its underlying mechanism. The heat treatment for 6–48 h induced apoptosis, potentiated caspase 3 activity, increased the expression levels of apoptosis-related gene BAX and ER stress markers, glucose-regulated protein 78 (GRP78), and CCAAT/enhancer binding protein homologous protein (CHOP) in mouse granulosa cells. The treatment with ER stress inhibitor 4-PBA significantly attenuated the adverse effects caused by CHS. Selenium treatment significantly attenuated the CHS- or thapsigargin (Tg, an ER stress activator)-induced apoptosis, potentiation of caspase 3 activity, and the increased protein expression levels of BAX, GRP78, and CHOP. Additionally, treatment of the cells with 5 ng/mL selenium significantly ameliorated the levels of estradiol, which were decreased in response to heat exposure. Consistently, administering selenium supplement alleviated the hyperthermia-caused reduction in the serum estradiol levels in vivo. Together, our findings indicate that selenium has protective effects on CHS-induced apoptosis via inhibition of the ER stress pathway. The current study provides new insights in understanding the role of selenium during the process of heat-induced cell apoptosis.

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Section: Discussionmentioning

confidence: 99%

“…Glucose-regulated protein 78 CHOP CCAAT/enhancer-binding protein (C/EBP) homologous protein CYP19A1 Cytochrome P450 family 19…”

Section: Hsmentioning

confidence: 99%

mentioning

confidence: 99%

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Selenium Attenuates Chronic Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in Mouse Granulosa Cells

et al. 2020

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“…Cells must overcome ERS to survive, but continuous ERS causes apoptosis . Research shows that continuous ERS can cause the activation of apoptosis‐related protein Bcl2‐like 11 (BIM) and p53‐upregulated modulator of apoptosis (PUMA), which then cause cytochrome C release, initiate the caspase cascade system and finally induce cell apoptosis …”

Section: Introductionmentioning

confidence: 99%

“…16 Research shows that continuous ERS can cause the activation of apoptosis-related protein Bcl2-like 11 (BIM) and p53-upregulated modulator of apoptosis (PUMA), which then cause cytochrome C release, initiate the caspase cascade system and finally induce cell apoptosis. 17 Proteasome 26S subunit non-ATPase 4 (PSMD4) contains a ubiquitin motif, which interacts with ubiquitination proteins to mediate protein degradation. 18 Related studies have found that deletion of the PSMD4 gene does not affect the survival of yeast, while in other organisms, development is affected by deletion of the PSMD4 gene.…”

Section: Introductionmentioning

confidence: 99%

PSMD4 regulates the malignancy of esophageal cancer cells by suppressing endoplasmic reticulum stress

Zhao

et al. 2019

The Kaohsiung J of Med Scie

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Proteasome 26S subunit non‐ATPase 4 (PSMD4) is an important proteasome ubiquitin receptor and plays a key role in endoplasmic reticulum stress (ERS). However, the study of PSMD4 in esophageal cancer (EC) is relatively rare. Here, we found that the expression of PSMD4 was markedly enhanced in EC tissues and cell lines. The cell counting kit‐8 (CCK‐8) assay showed that overexpression of PSMD4 significantly enhanced Eca109 cell viability, while inhibition of PSMD4 reduced Eca109 cell viability. Knockdown of PSMD4 induced Eca109 cell apoptosis and cell cycle arrest. More importantly, knockdown of PSMD4 significantly enhanced the expression of glucose regulated protein 78, activating transcription factor 6, and p‐protein kinase R‐like ER kinase, indicating an enhanced ERS response in esophageal cancer cells. Compared with the control cells, brefeldin A significantly inhibited the expression of PSMD4 and increased the expression of p53‐upregulated modulator of apoptosis. However, such effects were largely reversed after overexpressing PSMD4 in Eca109 cells, suggesting that silencing PSMD4 could enhance ERS‐induced cell apoptosis. In summary, upregulation of PSMD4 promoted the progression of esophageal cancer mainly by reducing ERS‐induced cell apoptosis.

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Adverse effects of cadmium on lymphoid organs, immune cells, and immunological responses

Kumari,

Nanda,

Firdaus

2024

J of Applied Toxicology

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Humans and animals possess robust immune systems to safeguard against foreign pathogens. However, recent reports suggest a greater incidence of immunity breakdown due to exposure to environmental pollutants, with heavy metals emerging as potential candidates in such immuno‐toxicological studies. While we have extensive data on the general toxicity resulting from exposure to heavy metals, comprehensive documentation of their role as immune disruptors remains scarce. Cd (Cadmium) exerts immunomodulation by interfering with immune organs and cells, leading to altered structure, physiology, and function, thereby inducing symptoms of immune deregulation, inflammation and/or autoimmunity.This review aims to summarize the link between Cd exposure and immune dysfunction, drawing from case studies on exposed human subjects, as well as research conducted on various model organisms and in‐vitro culture systems.

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Cadmium-induced endoplasmic reticulum stress in chicken neutrophils is alleviated by selenium

Cited by 41 publications

References 39 publications

Selenium Attenuates Chronic Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in Mouse Granulosa Cells

Selenium Attenuates Chronic Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in Mouse Granulosa Cells

PSMD4 regulates the malignancy of esophageal cancer cells by suppressing endoplasmic reticulum stress

Adverse effects of cadmium on lymphoid organs, immune cells, and immunological responses

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