Interaction of SiO2 nanoparticles with neuronal cells: Ionic mechanisms involved in the perturbation of calcium homeostasis

Gilardino, Alessandra; Catalano, Federico; Alberto, Gabriele; Nilius, Bernd; Antoniotti, Susanna; Martra, Gianmario; Lovisolo, Davide

doi:10.1016/j.biocel.2015.07.012

Cited by 33 publications

(47 citation statements)

References 56 publications

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“…Moreover, as shown in Fig. 4G, the T-type channel protein was not detected either in GN11 or in 994-D4 cells, while it was present in GT1-7 cells, that have been shown to possess functional T-type channels [23]. Therefore, proteins levels are not univocally related to transcript levels, and this is not unexpected, given the complex regulatory pathways controlled by REST, both at the transcriptional and post-transcriptional level [3].…”

Section: L-and P/q-type Channel Expressionmentioning

confidence: 78%

REST levels affect the functional expression of voltage dependent calcium channels and the migratory activity in immortalized GnRH neurons

Antoniotti

Torriano

Luganini

et al. 2016

Neuroscience Letters

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REST levels affect the functional expression of voltage dependent calcium channels and the migratory activity in immortalized GnRH neurons, Neuroscience Letters http://dx.doi.org/10. 1016/j.neulet.2016.06.050 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. We downregulated REST transcription factor in neuronal GN11 cell line by silencing.994-D4 clone, expressing low REST levels, showed a reduced migratory potential.REST silencing increased expression of functional voltage-dependent Ca 2+ channels.Enhancement of depolarization-induced calcium signals is dependent on P/Q channels 3 Abbreviations:REST/NRSF, repressor element-1 silencing transcription factor/neuron restrictive silencer factor; VDCCs, voltage dependent calcium channels; GnRH, gonadotropin hormone-releasing hormone.4 AbstractThe repressor element-1 silencing transcription factor (REST) has emerged as a key controller of neuronal differentiation and has been shown to play a critical role in the expression of the neuronal phenotype; however, much has still to be learned about its role at specific developmental stages and about the functional targets affected. Among these targets, calcium signaling mechanisms are critically dependent on the developmental stage and their full expression is a hallmark of the mature, functional neuron. We have analyzed the role played by REST in GN11 cells, an immortalized cell line derived from gonadotropin hormone releasing hormone (GnRH) neurons at an early developmental stage, electrically non-excitable and with a strong migratory activity. We show for the first time that functional voltage-dependent calcium channels are expressed in wild type GN11 cells; down-regulation of REST by a silencing approach shifts these cells towards a more differentiated phenotype, increasing the functional expression of P/Q-type channels and reducing their migratory potential.

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Section: L-and P/q-type Channel Expressionmentioning

confidence: 78%

REST levels affect the functional expression of voltage dependent calcium channels and the migratory activity in immortalized GnRH neurons

Antoniotti

Torriano

Luganini

et al. 2016

Neuroscience Letters

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“…That nanoparticles can have a regulatory impact on ion channels was shown for SiO 2 nanoparticles on TRP4 channels in a neuronal cell line. 52 Ion channels are tightly connected to the cytoskeleton, especially to the actin fibers, 19 either through bindings between specialized proteins and the fibers 53 or through interaction between fibers and lipid rafts, in which the channels can be located. 20 These connections allow the channels to maintain their function in the fluidic environment of the membrane.…”

Section: Discussionmentioning

confidence: 99%

Comparison of cellular effects of starch-coated SPIONs and poly(lactic-co-glycolic acid) matrix nanoparticles on human monocytes

Gonnissen¹,

Qu²,

Langer³

et al. 2016

IJN

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Within the last years, progress has been made in the knowledge of the properties of medically used nanoparticles and their toxic effects, but still, little is known about their influence on cellular processes of immune cells. The aim of our comparative study was to present the influence of two different nanoparticle types on subcellular processes of primary monocytes and the leukemic monocyte cell line MM6. We used core-shell starch-coated superparamagnetic iron oxide nanoparticles (SPIONs) and matrix poly(lactic-co-glycolic acid) (PLGA) nanoparticles for our experiments. In addition to typical biocompatibility testing like the detection of necrosis or secretion of interleukins (ILs), we investigated the impact of these nanoparticles on the actin cytoskeleton and the two voltage-gated potassium channels Kv1.3 and Kv7.1. Induction of necrosis was not seen for PLGA nanoparticles and SPIONs in primary monocytes and MM6 cells. Likewise, no alteration in secretion of IL-1β and IL-10 was detected under the same experimental conditions. In contrast, IL-6 secretion was exclusively downregulated in primary monocytes after contact with both nanoparticles. Two-electrode voltage clamp experiments revealed that both nanoparticles reduce currents of the aforementioned potassium channels. The two nanoparticles differed significantly in their impact on the actin cytoskeleton, demonstrated via atomic force microscopy elasticity measurement and phalloidin staining. While SPIONs led to the disruption of the respective cytoskeleton, PLGA did not show any influence in both experimental setups. The difference in the effects on ion channels and the actin cytoskeleton suggests that nanoparticles affect these subcellular components via different pathways. Our data indicate that the alteration of the cytoskeleton and the effect on ion channels are new parameters that describe the influence of nanoparticles on cells. The results are highly relevant for medical application and further evaluation of nanomaterial biosafety.

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“…Novel self-assembly nanoparticles showed promising results to bypass the blood-brain barrier and induce wide neuronal response using Gold or Albumin [35], [36], [37]. However, in the case of regulating astrocyte intracellular Ca 2+ through IP 3 control, we need to possibly design these self-assembly nanoparticles based on Carbon Black, Titanium Dioxide or Zinc Oxide [38], [39]. Even though promising, the usage of these nanoparticles increase toxicity levels in the cell, and their in-vivo applicability remains an interesting research challenge [40].…”

Section: A Prevention Of Neurodegenerative Diseasesmentioning

confidence: 99%

Feed-Forward and Feedback Control in Astrocytes for Ca2+-Based Molecular Communications Nanonetworks

Barros

Dey

2020

IEEE/ACM Trans. Comput. Biol. and Bioinf.

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Synaptic plasticity depends on the gliotransmitters' concentration in the synaptic channel. And, an abnormal concentration of gliotransmitters is linked to neurodegenerative diseases, including Alzheimer's, Parkinson's, and epilepsy. In this paper, a theoretical investigation of the cause of the abnormal concentration of gliotransmitters and how to achieve its control is presented through a Ca 2+-signalling-based molecular communications framework. A feed-forward and feedback control technique is used to manipulate IP3 values to stabilise the concentration of Ca 2+ inside the astrocytes. The theoretical analysis of the given model aims i) to stabilize the Ca 2+ concentration around a particular desired level in order to prevent abnormal gliotransmitters' concentration (extremely high or low concentration can result in neurodegeneration), ii) to improve the molecular communication performance that utilises Ca 2+ signalling, and maintain gliotransmitters' regulation remotely. It shows that the refractory periods from Ca 2+ can be maintained to lower the noise propagation resulting in smaller time-slots for bit transmission, which can also improve the delay and gain performances. The proposed approach can potentially lead to novel nanomedicine solutions for the treatment of neurodegenerative diseases, where a combination of nanotechnology and gene therapy approaches can be used to elicit the regulated Ca 2+ signalling in astrocytes, ultimately improving neuronal activity.

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Interaction of SiO2 nanoparticles with neuronal cells: Ionic mechanisms involved in the perturbation of calcium homeostasis

Cited by 33 publications

References 56 publications

REST levels affect the functional expression of voltage dependent calcium channels and the migratory activity in immortalized GnRH neurons

REST levels affect the functional expression of voltage dependent calcium channels and the migratory activity in immortalized GnRH neurons

Comparison of cellular effects of starch-coated SPIONs and poly(lactic-co-glycolic acid) matrix nanoparticles on human monocytes

Feed-Forward and Feedback Control in Astrocytes for Ca2+-Based Molecular Communications Nanonetworks

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