Loss of gap junctional intercellular communication in rat lung epithelial cells exposed to carbon or silica-based nanoparticles

Ale‐Agha, Niloofar; Albrecht, Catrin; Klotz, Lars‐Oliver

doi:10.1515/bc.2010.133

Cited by 18 publications

(12 citation statements)

References 39 publications

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“…2 that could be the cause of the observed increase in migration of cells. Similarly, uptake of similarly sized MNPs has been reported to decrease intercellular gap junction communication (40). This work found that stress kinases and β-catenin levels modulate the alterations in intercellular gap junction communication.…”

Section: Discussionmentioning

confidence: 96%

Force Dependent Internalization of Magnetic Nanoparticles Results in Highly Loaded Endothelial Cells for Use as Potential Therapy Delivery Vectors

2012

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Purpose To investigate the kinetics, mechanism and extent of MNP loading into endothelial cells and the effect of this loading on cell function. Methods MNP uptake was examined under field on/off conditions, utilizing varying magnetite concentration MNPs. MNP-loaded cell viability and functional integrity was assessed using metabolic respiration, cell proliferation and migration assays. Results MNP uptake in endothelial cells significantly increased under the influence of a magnetic field versus non-magnetic conditions. Larger magnetite density of the MNPs led to a higher MNP internalization by cells under application of a magnetic field without compromising cellular respiration activity. Two-dimensional migration assays at no field showed that higher magnetite loading resulted in greater cell migration rates. In a three-dimensional migration assay under magnetic field, the migration rate of MNP-loaded cells was more than twice that of unloaded cells and was comparable to migration stimulated by a serum gradient. Conclusions Our results suggest that endothelial cell uptake of MNPs is a force dependent process. The in vitro assays determined that cell health is not adversely affected by high MNP loadings, allowing these highly magnetically responsive cells to be potentially beneficial therapy (gene, drug or cell) delivery systems.

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Section: Discussionmentioning

confidence: 96%

Force Dependent Internalization of Magnetic Nanoparticles Results in Highly Loaded Endothelial Cells for Use as Potential Therapy Delivery Vectors

2012

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“…After the treatment with ultrafine SiO NPs, GJIC decreased by 77%, indicating the reduction in intercellular communication and signaling. [147]…”

Section: Biocompatibility Assessment For Si and Sio Particlesmentioning

confidence: 99%

“…[190] After the exposure to SiO particles (14 nm), Ale-Agha et al observed changes in the subcellular localization of connexin-43 and of β-catenin, proteins for gap junctional intercellular communication, in rat lung epithelial cells (RLE). [147] Interestingly, Huang et al reported that mesoporous SiO NPs decreased ROS production in human malignant melanoma cells (A375), a skin cancer cell line, but adversely caused an increase in cancer cell proliferation. [201] While these few described studies exhibit minor evidence of genotoxicity, it is still unknown whether the oxidative stress formed was through direct or indirect mechanisms.…”

Section: Genotoxicity Of Sio Particlesmentioning

confidence: 99%

Biocompatibility assessment of Si-based nano- and micro-particles

Jaganathan

Godin

2012

Advanced Drug Delivery Reviews

227

131

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Silicon is one of the most abundant chemical elements found on the Earth. Due to its unique chemical and physical properties, silicon based materials and their oxides (e.g. silica) have been used in several industries such as building and construction, electronics, food industry, consumer products and biomedical engineering/medicine. This review summarizes studies on effects of silicon and silica nano- and micro-particles on cells and organs following four main exposure routes, namely, intravenous, pulmonary, dermal and oral. Further, possible genotoxic effects of silica based nanoparticles are discussed. The review concludes with an outlook on improving and standardizing biocompatibility assessment for nano- and micro-particles.

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“…Cell death receptors could also be induced by nanomaterials as discussed above. CB nanoparticles induce EGFR signaling leading to disruption of gap junctional intercellular communication 4,48 , cell proliferation and apoptosis 15 . CB nanoparticles may however activate EGFR indirectly through ROS production and activation of lipid raft signaling 49 .…”

Section: Consequences Of the Interaction Of Nanomaterials With Proteinsmentioning

confidence: 99%

Carbon black and titanium dioxide nanoparticles induce distinct molecular mechanisms of toxicity

Boland

Hussain

Baeza‐Squiban

2014

WIREs Nanomed Nanobiotechnol

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Increasing evidence link nanomaterials with adverse biological outcomes and due to the variety of applications and potential human exposures to nanoparticles it is thus important to evaluate their toxicity for the risk assessment of workers and consumers. It is crucial to understand the underlying mechanisms of their toxicity as observation of similar effects after different nanomaterial exposures does not reflect similar intracellular processing and organelle interactions. A thorough understanding of mechanisms is not only needed for accurate prediction of potential toxicological impacts but also for the development of safer nanoapplications by modulating the physico-chemical characteristics. Furthermore biomedical applications may also take advantage of an in depth knowledge about the mode of action of nanotoxicity to design new nanoparticle-derived drugs. In the present manuscript we discuss the similarities and differences in molecular pathways of toxicity after carbon black and TiO2 nanoparticle exposures and identify the main toxicity mechanisms induced by these two nanoparticles which may also be indicative for the mode of action of other insoluble nanomaterials. We address the translocation, cell death induction, genotoxicity and inflammation induced by titanium dioxide and carbon black nanoparticles which depend on their internalisation, ROS production capacities and/or protein interactions. We summarise their distinct cellular mechanisms of toxicity and the crucial steps which may be targeted to avoid adverse effects or to induce them for nanomedical purposes. Several physico-chemical characteristics could influence these general toxicity pathways depicted here and the identification of common toxicity pathways could support the grouping of nanomaterials in terms of toxicity.

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Loss of gap junctional intercellular communication in rat lung epithelial cells exposed to carbon or silica-based nanoparticles

Cited by 18 publications

References 39 publications

Force Dependent Internalization of Magnetic Nanoparticles Results in Highly Loaded Endothelial Cells for Use as Potential Therapy Delivery Vectors

Force Dependent Internalization of Magnetic Nanoparticles Results in Highly Loaded Endothelial Cells for Use as Potential Therapy Delivery Vectors

Biocompatibility assessment of Si-based nano- and micro-particles

Carbon black and titanium dioxide nanoparticles induce distinct molecular mechanisms of toxicity

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