Endoplasmic reticulum stress signaling is involved in silver nanoparticles-induced apoptosis

Zhang, Rui; Piao, Mei Jing; Kim, Ki Cheon; Kim, Areum Daseul; Choi, Jeong‐Yun; Choi, Jinhee; Hyun, Jin Won

doi:10.1016/j.biocel.2011.10.019

Cited by 142 publications

(118 citation statements)

References 63 publications

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“…In conclusion, our results validate that high dose of CdTe QDs (10 µg/mL, close to the TC 50 obtained from our previous results 19 ) might cause severe pro-apoptotic ER stress response. Combined with previous report, 45,46 our data also suggest that NPs-induced ER stress may be a common cellular response to nanomaterials in various cell types. In addition, the lower dosage could be considered as a warning to the following realistic damage outcomes.…”

supporting

confidence: 89%

Cytotoxicity of CdTe quantum dots in human umbilical vein endothelial cells: the involvement of cellular uptake and induction of pro-apoptotic endoplasmic reticulum stress

Yan

Zhang

Qin

et al. 2016

IJN

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Cadmium telluride quantum dots (CdTe QDs) have been proposed to induce oxidative stress, which plays a crucial role in CdTe QDs-mediated mitochondrial-dependent apoptosis in human umbilical vein endothelial cells (HUVECs). However, the direct interactions of CdTe QDs with HUVECs and their potential impairment of other organelles like endoplasmic reticulum (ER) in HUVECs are poorly understood. In this study, we reported that the negatively charged CdTe QDs (−21.63±0.91 mV), with good dispersity and fluorescence stability, were rapidly internalized via endocytosis by HUVECs, as the notable internalization could be inhibited up to 95.52% by energy depletion (NaN 3 /deoxyglucose or low temperature). The endocytosis inhibitors (methyl-β-cyclodextrin, genistein, sucrose, chlorpromazine, and colchicine) dramatically decreased the uptake of CdTe QDs by HUVECs, suggesting that both caveolae/raft- and clathrin-mediated endocytosis were involved in the endothelial uptake of CdTe QDs. Using immunocytochemistry, a striking overlap of the internalized CdTe QDs and ER marker was observed, which indicates that QDs may be transported to ER. The CdTe QDs also caused remarkable ER stress responses in HUVECs, confirmed by significant dilatation of ER cisternae, upregulation of ER stress markers GRP78/GRP94, and activation of protein kinase RNA-like ER kinase-eIF2α-activating transcription factor 4 pathway (including phosphorylation of both protein kinase RNA-like ER kinase and eIF2α and elevated level of activating transcription factor 4). CdTe QDs further promoted an increased C/EBP homologous protein expression, phosphorylation of c-JUN NH2-terminal kinase, and cleavage of ER-resident caspase-4, while the specific inhibitor (SP600125, Z-LEVD-fmk, or salubrinal) significantly attenuated QDs-triggered apoptosis, indicating that all three ER stress-mediated apoptosis pathways were activated and the direct participation of ER in the CdTe QDs-caused apoptotic cell death in HUVECs. Our findings provide important new insights into QDs toxicity and reveal potential cardiovascular risks for the future applications of QDs.

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supporting

confidence: 89%

Cytotoxicity of CdTe quantum dots in human umbilical vein endothelial cells: the involvement of cellular uptake and induction of pro-apoptotic endoplasmic reticulum stress

Yan

Zhang

Qin

et al. 2016

IJN

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“…wed in Djur n D (Zhang et al 2012, Chen et al 2014, Yu, Chang, et al 2015. Our data show that the internalization of titanium (TiO 2 NPs), besides increasing the cell calcium content, does also induce the expression of CHOP (ATF4 pathway) and activates (i) the ER stress in HUVEC cells and (ii) differentiation in keratinocytes.…”

Section: Previous Studie Previous Stumentioning

confidence: 77%

“…Our data show that the internalization of titanium (TiO 2 NPs), besides increasing the cell calcium content, does also induce the expression of CHOP (ATF4 pathway) and activates (i) the ER stress in HUVEC cells and (ii) differentiation in keratinocytes. In addition, ER stress and disruption of cellular calcium homeostasis are strongly associated with mitochondrial dysfunction (Zhang et al 2012). Here, we show that this mitochondrial alteration is effective for a minimal content of TiO 2 NPs defining here the level of toxicity.…”

Section: Previous Studie Previous Stumentioning

confidence: 87%

“…Recent studies report the endoplasmic reticulum stress (ER stress) as a common response in NPs related toxicity with studies on TiO 2 NPs (Zhang et al 2012, Chen et al 2014, Yu, Chang, et al 2015. The endoplasmic reticulum (ER) is an important organelle, which plays a role in folding and assembling of cellular proteins, in synthesis of lipids and sterols, and in regulating the balance of the intracellular calcium homeostasis, processes which are all dependent on the ER internal homeostasis.…”

Section: Introductionmentioning

confidence: 99%

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In situquantification of diverse titanium dioxide nanoparticles unveils selective endoplasmic reticulum stress-dependent toxicity

et al. 2017

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“…Different types of nanoparticles were shown to induce ER stress response, including zinc oxide (10). However, only a few studies reported that AgNP can induce ER stress events in zebrafish and in human Chang liver cells (11,12).…”

Section: Discussionmentioning

confidence: 99%

Silver Nanoparticles Induce Degradation of the Endoplasmic Reticulum Stress Sensor Activating Transcription Factor-6 Leading to Activation of the NLRP-3 Inflammasome

Simard

Vallières

Liz

et al. 2015

Journal of Biological Chemistry

115

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Background: Some nanoparticles are known to induce endoplasmic reticulum (ER) stress and lead to cell death. Results: Silver nanoparticles induce ATF-6 degradation, leading to activation of the NLRP-3 inflammasome and pyroptosis. Conclusion: ATF-6 is an important target to silver nanoparticles. Significance: Our results provide a new link between ER stress and activation of the NLRP-3 inflammasome.

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Endoplasmic reticulum stress signaling is involved in silver nanoparticles-induced apoptosis

Cited by 142 publications

References 63 publications

Cytotoxicity of CdTe quantum dots in human umbilical vein endothelial cells: the involvement of cellular uptake and induction of pro-apoptotic endoplasmic reticulum stress

Cytotoxicity of CdTe quantum dots in human umbilical vein endothelial cells: the involvement of cellular uptake and induction of pro-apoptotic endoplasmic reticulum stress

In situquantification of diverse titanium dioxide nanoparticles unveils selective endoplasmic reticulum stress-dependent toxicity

Silver Nanoparticles Induce Degradation of the Endoplasmic Reticulum Stress Sensor Activating Transcription Factor-6 Leading to Activation of the NLRP-3 Inflammasome

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