Endoplasmic reticulum stress and alteration in calcium homeostasis are involved in cadmium-induced apoptosis

Biagioli, Marta; Pifferi, Simone; Ragghianti, Matilde; Bucci, Stefania; Meneghesso, Gaudenzio; Pinton, Paolo

doi:10.1016/j.ceca.2007.05.003

Cited by 159 publications

(112 citation statements)

References 52 publications

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“…In line with the previous reports (Biagioli et al, 2008;Wang et al, 2009;Xu et al, 2011) Misra et al (2003) an increase in IP3, an ligand of IP3R following exposure to cadmium suggests that cadmium could activate IP3R through increase of intracellular IP3 which then causes release of calcium from ER which is an major calcium storage compartment of the cell. Pre-treatment with an inhibitor of the calcium channel of ER (IP3R) suggests that the release of calcium from ER in stimulating apoptosis (Deniaud et al, 2008).…”

Section: Discussionsupporting

confidence: 91%

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Lin¹,

Peng²,

Yang³

et al. 2015

Bangladesh J Pharmacol

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Cadmium, a toxic environmental contaminant, induces oxidative stress leading to various neurodegenerative disorders, where it interferes with homeos-tasis of intracellular free calcium ([Ca2+]i), leading to cellular damage and apoptosis. We investigated whether resveratrol, a plant-derived antioxidant could offer protection against cadmium-induced neuroapoptosis. Primary cortical neurons were exposed to cadmium (10 or 20 µM) with/without prior exposure to resveratrol (5, 10 or 20 µM) for 12 hours and unexposed cells served as control. Resveratrol caused marked reduction in cadmium-induced neuronal apoptosis and down-regulated caspase-3 expressions. Cadmium-induced marked elevations in reactive oxygen species, and ([Ca2+]i) levels were potentially reduced by resveratrol. Resveratrol effectively regulated the alterations observed in the activation levels of mitogen-activated protein kinases (MAPKs) and proteins of mammalian target of rapamycin (mTOR) pathways. Thus, resveratrol effectively protected the cortical neurons exposed to cadmium by modulating the ([Ca2+]i) levels and regulating the MAPK/mTOR pathways.

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Section: Discussionsupporting

confidence: 91%

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Lin¹,

Peng²,

Yang³

et al. 2015

Bangladesh J Pharmacol

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“…Cadmium causes ER stress in vitro and in vivo and mediates induction of apoptosis in some tissues [79]. However, to date no conclusive data are available in Cd-induced ER stress and its relation with hepatocyte apoptosis [80,81] (Figure 3). …”

Section: Cadmium-induced Apoptosismentioning

confidence: 99%

Liver and Cadmium Toxicity

2013

J Drug Metab Toxicol

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“…ers-induced apoptosis has been implicated in several diseases such as diabetes mellitus, parkinson's disease (15) and has been demonstrated in some tumor cell lines such as pc-12 neuronal cells (16) and lung carcinoma A-549 cells (17). Some drugs, ischemia-reperfusion, hypoxia and glucose starvation can disturb er function and may lead to ers (18)(19)(20). ERS initiates the unfolded protein response (UPR), which alleviates protein overload in the er (21).…”

Section: Introductionmentioning

confidence: 99%

Involvement of endoplasmic reticulum stress in adenosine-induced human hepatoma HepG2 cell apoptosis

Ye²,

Huang³

et al. 2011

Oncol Rep

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Abstract. endoplasmic reticulum stress (ers)-mediated cell apoptosis has been implicated in the development of multiple diseases such as cancer, neurodegenerative diseases and ischemic reperfusion damage. previous studies have demonstrated the adenosine-induced apoptosis in several tumor cell lines. However, the role of ers in adenosine-induced human hepatoma Hepg2 cell apoptosis remains unclear. the present study was designed to determine whether ers is involved in adenosine-induced Hepg2 cell apoptosis. the Mtt assay was used to determine proliferation, and DApI staining of cell nuclei was performed to determine cell apoptosis. the translocation of cHop and caspase-3 was observed by immunofluorescence analysis, and the protein expression of CHOP, caspase-4 and caspase-3 was detected by Western blotting. the Mtt assay demonstrated that adenosine inhibited Hepg2 cell proliferation in a dose-dependent manner. DApI staining of cell nuclei and cell cycle analysis verified cell apoptosis. The immunofluorescence assay demonstrated that adenosine induced the translocation of cHop and of caspase-3 from the cytoplasm to the nucleus. Western blotting confirmed that cHop, caspase-4 and caspase-3 were up-regulated in Hepg2 cells after treatment with adenosine. However, JnK protein expression was not altered. These results show that ERS is involved in the adenosine-induced Hepg2 cell apoptosis.

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Endoplasmic reticulum stress and alteration in calcium homeostasis are involved in cadmium-induced apoptosis

Cited by 159 publications

References 52 publications

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Liver and Cadmium Toxicity

Involvement of endoplasmic reticulum stress in adenosine-induced human hepatoma HepG2 cell apoptosis

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