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8. Internalisation of engineered nanoparticles into mammalian cells in vitro: influence of cell type and particle properties

Author

Busch, Wibke, Bastian, S., Trahorsch, Ulrike, Iwe, M., Kühnel, Dana, Meißner, T., Springer, A., Gelinsky, M., Richter, V., Ikonomidou, C., Potthoff, A., Lehmann, Irina, Schirmer, K., Busch, Wibke, Bastian, S., Trahorsch, Ulrike, Iwe, M., Kühnel, Dana, Meißner, T., Springer, A., Gelinsky, M., Richter, V., Ikonomidou, C., Potthoff, A., Lehmann, Irina, and Schirmer, K.

Abstract

Cellular internalisation of industrial engineered nanoparticles is undesired and a reason for concern. Here we investigated and compared the ability of seven different mammalian cell cultures in vitro to incorporate six kinds of engineered nanoparticles, focussing on the role of cell type and particle properties in particle uptake. Uptake was examined using light and electron microscopy coupled with energy dispersive X-ray spectroscopy (EDX) for particle element identification. Flow cytometry was applied for semi-quantitative analyses of particle uptake and for exploring the influence on uptake by the phagocytosis inhibitor Cytochalasin D (CytoD). All particles studied were found to enter each kind of cultured cells. Yet, particles were never found within cell nuclei. The presence of the respective particles within the cells was confirmed by EDX. Live-cell imaging revealed the time-dependent process of internalisation of technical nanoparticles, which was exemplified by tungsten carbide particle uptake into the human skin cells, HaCaT. Particles were found to co-localise with lysosomal structures within the cells. The incorporated nanoparticles changed the cellular granularity, as measured by flow cytometry, already after 3 h of exposure in a particle specific manner. By correlating particle properties with flow cytometry data, only the primary particle size was found to be a weakly influential property for particle uptake. CytoD, an inhibitor of actin filaments and therewith of phagocytosis, significantly inhibited the internalisation of particle uptake in only two of the seven investigated cell cultures. Our study, therefore, supports the notion that nanoparticles can enter mammalian cells quickly and easily, irrespective of the phagocytic ability of the cells.

Published
2011

10. Morphological and neurocognitive sequelae following chemotherapy for leukemia in early childhood

Author

Genschaft, M, primary, Hübner, T, additional, Plessow, F, additional, Krone, F, additional, Ikonomidou, VN, additional, Abolmaali, A, additional, Gruhn, B, additional, Hernaiz, P, additional, Hofmann, A, additional, Holfeld, E, additional, Kramm, P, additional, Vorwerk, P, additional, Hummel, T, additional, Ikonomidou, C, additional, Kirschbaum, C, additional, Smolka, MN, additional, and Suttorp, M, additional

Published
2011
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11. P09.3 Morphological and neurocognitive sequelae following chemotherapy for leukemia in early childhood

Author

Genschaft, M., primary, Hübner, T., additional, Plessow, F., additional, Krone, F., additional, Ikonomidou, V.N., additional, Abolmaali, N., additional, Hoffmann, A., additional, Holfeld, E., additional, Vorwerk, P., additional, Kramm, C., additional, Gruhn, B., additional, Hernaiz-Driever, P., additional, Suttorp, M., additional, Hummel, T., additional, Ikonomidou, C., additional, Kirschbaum, C., additional, and Smolka, M.N., additional

Published
2011
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12. Suppression of the Intrinsic Apoptosis Pathway by Synaptic Activity

Author

Leveille, F., primary, Papadia, S., additional, Fricker, M., additional, Bell, K. F. S., additional, Soriano, F. X., additional, Martel, M.-A., additional, Puddifoot, C., additional, Habel, M., additional, Wyllie, D. J., additional, Ikonomidou, C., additional, Tolkovsky, A. M., additional, and Hardingham, G. E., additional

Published
2010
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14. Accumulation of the anandamide precursor and other N-acylethanolamine phospholipids in infant rat models of in vivo necrotic and apoptotic neuronal death

Author

Hansen, H.H., Ikonomidou, C., Bittigau, P., Hansen, S.H., Hansen, Harald S., Hansen, H.H., Ikonomidou, C., Bittigau, P., Hansen, S.H., and Hansen, Harald S.

Abstract

It has been demonstrated that the endogenous cannabinoid receptor ligand, anandamide, and other N-acylethanolamines (NAEs), accumulate during neuronal injury in vitro, a process that may be linked to the neuroprotective effects of NAEs. The crucial step for generation of NAEs is the synthesis of the corresponding precursors, N-acylethanolamine phospholipids (NAPEs). However, it is unknown whether this key event for NAE formation is regulated differently in the context of insults causing necrotic or apoptotic neuronal death. To address this question, we monitored a range of Cortical NAPE species in three infant rat models of in vivo neurodegeneration: (i) necrosis caused by intrastriatal injection of NMDA (25 nmol); (ii) apoptosis induced by systemic administration of the NMDA-receptor antagonist (+)MK-801 (3 × 0.5 mg/kg, i.p.); and (iii) apoptosis following focal necrosis triggered by concussive head trauma. A marked increase of all NAPE species was observed in both hemispheres 4 and 24 h after NMDA-induced injury, with a relatively larger increase in N-stearoyl-containing NAPE species. Thus, the percentage of the anandamide precursor fell from 1.1 to 0.5 mol%. In contrast, administration of (+)MK-801 did not alter cortical NAPE levels. Concussion head trauma resulted in a similar but less pronounced upregulation of NAPE levels at both 4 and 24 h as compared to NMDA injections. Increased levels of NAPE 24 h post-trauma possibly reflect that necrosis is still ongoing at this time point. Consequently, our data suggest that excitotoxic necrotic mechanisms of neurodegeneration, as opposed to apoptotic neurodegeneration, have a profound effect on in vivo NAE precursor homeostasis.

Published
2001

15. Anandamide, but not 2-arachidonoylglycerol, accumulates during in vivo neurodegeneration

Author

Hansen, H.H., Lastres-Becker, I., Berrendero, F., Manzanares, J., Javier Fernández-Ruiz, J., Schmid, P.C., Schmid, H.H.O., Bittigau, P., Ikonomidou, C., Hansen, Harald S., Hansen, H.H., Lastres-Becker, I., Berrendero, F., Manzanares, J., Javier Fernández-Ruiz, J., Schmid, P.C., Schmid, H.H.O., Bittigau, P., Ikonomidou, C., and Hansen, Harald S.

Abstract

Endogenous cannabinoid receptor ligands (endocannabinoids) may rescue neurons from glutamate excitotoxicity. As these substances also accumulate in cultured immature neurons following neuronal damage, elevated endocannabinoid concentrations may be interpreted as a putative neuroprotective response. However, it is not known how glutamatergic insults affect in vivo endocannabinoid homeostasis, i.e. N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG), as well as other constituents of their lipid families, N-acylethanolamines (NAEs) and 2-monoacylglycerols (2-MAGs), respectively. Here we employed three in vivo neonatal rat models characterized by widespread neurodegeneration as a consequence of altered glutamatergic neurotransmission and assessed changes in endocannabinoid homeostasis. A 46-fold increase of cortical NAE concentrations (anandamide, 13-fold) was noted 24 h after intracerebral NMDA injection, while less severe insults triggered by mild concussive head trauma or NMDA receptor blockade produced a less pronounced NAE accumulation. By contrast, levels of 2-AG and other 2-MAGs were virtually unaffected by the insults employed, rendering it likely that key enzymes in biosynthetic pathways of the two different endocannabinoid structures are not equally associated to intracellular events that cause neuronal damage in vivo. Analysis of cannabinoid CB receptor mRNA expression and binding capacity revealed that cortical subfields exhibited an up-regulation of these parameters following mild concussive head trauma and exposure to NMDA receptor blockade. This may suggest that mild to moderate brain injury may trigger elevated endocannabinoid activity via concomitant increase of anandamide levels, but not 2-AG, and CB receptor density.

Published
2001

35. Expanding the phenotypic spectrum of lupus erythematosus in Aicardi-Goutières syndrome.

Author

Ramantani G, Kohlhase J, Hertzberg C, Innes AM, Engel K, Hunger S, Borozdin W, Mah JK, Ungerath K, Walkenhorst H, Richardt HH, Buckard J, Bevot A, Siegel C, von Stülpnagel C, Ikonomidou C, Thomas K, Proud V, Niemann F, and Wieczorek D

Abstract

OBJECTIVE: Aicardi-Goutières syndrome (AGS) is an early-onset encephalopathy resembling congenital viral infection that is characterized by basal ganglia calcifications, loss of white matter, cerebrospinal fluid (CSF) lymphocytosis, and elevated interferon-alpha levels in the CSF. Studies have shown that AGS is an autosomal-recessive disease linked to mutations in 5 genes, encoding the 3'-repair DNA exonuclease 1 (TREX1), the 3 subunits of ribonuclease H2 (RNASEH2A-C), and sterile alpha motif domain and HD domain-containing protein 1 (SAMHD1). In this study we further characterized the phenotypic spectrum of this disease. METHODS: Clinical and laboratory data were obtained from 26 patients fulfilling the clinical diagnostic criteria for AGS. Genomic DNA was screened for mutations in all 5 AGS genes by direct sequencing, and sera were analyzed for autoantibodies. RESULTS: In 20 patients with AGS, 20 mutations, 12 of which were novel, were identified in all 5 AGS genes. Clinical and laboratory investigations revealed a high prevalence of features (some not previously described in patients with AGS) that are commonly seen in patients with systemic lupus erythematosus (SLE), such as thrombocytopenia, leukocytopenia, antinuclear antibodies, erythematous lesions, oral ulcers, and arthritis, which were observed in 12 (60%) of 20 patients with AGS. Moreover, the coexistence of AGS and SLE, was for the first time, demonstrated in 2 patients with molecularly proven AGS. CONCLUSION: These findings expand the phenotypic spectrum of lupus erythematosus in AGS and provide further insight into its disease mechanisms by showing that activation of the innate immune system as a result of inherited defects in nucleic acid metabolism could lead to systemic autoimmunity. [ABSTRACT FROM AUTHOR]

Published
2010
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37. Toxicity of tungsten carbide and cobalt-doped tungsten carbide nanoparticles in mammalian cells in vitro.

Author

Bastian S, Busch W, Kühnel D, Springer A, Meißner T, Holke R, Scholz S, Iwe M, Pompe W, Gelinsky M, Potthoff A, Richter V, Ikonomidou C, and Schirmer K

Abstract

Background: Tungsten carbide nanoparticles are being explored for their use in the manufacture of hard metals. To develop nanoparticles for broad applications, potential risks to human health and the environment should be evaluated and taken into consideration. Objective: We aimed to assess the toxicity of well-characterized tungsten carbide (WC) and cobaltdoped tungsten carbide (WC-Co) nanoparticle suspensions in an array of mammalian cells. Methods: We examined acute toxicity of WC and of WC-Co (10% weight content Co) nanoparticles in different human cell lines (lung, skin, and colon) as well as in rat neuronal and glial cells (i.e., primary neuronal and astroglial cultures and the oligodendrocyte precursor cell line OLN-93). Furthermore, using electron microscopy, we assessed whether nanoparticles can be taken up by living cells. We chose these in vitro systems in order to evaluate for potential toxicity of the nanoparticles in different mammalian organs (i.e., lung, skin, intestine, and brain). Results: Chemical-physical characterization confirmed that WC as well as WC-Co nanoparticles with a mean particle size of 145 nm form stable suspensions in serum-containing cell culture media. WC nanoparticles were not acutely toxic to the studied cell lines. However, cytotoxicity became apparent when particles were doped with Co. The most sensitive were astrocytes and colon epithelial cells. Cytotoxicity of WC-Co nanoparticles was higher than expected based on the ionic Co content of the particles. Analysis by electron microscopy demonstrated presence of WC nanoparticles within mammalian cells. Conclusions: Our findings demonstrate that doping of WC nanoparticles with Co markedly increases their cytotoxic effect and that the presence of WC-Co in particulate form is essential to elicit this combinatorial effect. [ABSTRACT FROM AUTHOR]

Published
2009
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38. Acute and long-term proteome changes induced by oxidative stress in the developing brain.

Author

Kaindl, A. M., Sifringer, M., Zabel, C., Nebrich, G., Wacker, M. A., Felderhoff-Mueser, U., Endesfelder, S., von der Hagen, M., Stefovska, V., Klose, J., and Ikonomidou, C.

Subjects
OXIDATIVE stress, BRAIN, PROTEOMICS, CARBONYL compounds, CELL proliferation, APOPTOSIS
Abstract

The developing mammalian brain experiences a period of rapid growth during which various otherwise innocuous environmental factors cause widespread apoptotic neuronal death. To gain insight into developmental events influenced by a premature exposure to high oxygen levels and identify proteins engaged in neurodegenerative and reparative processes, we analyzed mouse brain proteome changes at P7, P14 and P35 caused by an exposure to hyperoxia at P6. Changes detected in the brain proteome suggested that hyperoxia leads to oxidative stress and apoptotic neuronal death. These changes were consistent with results of histological and biochemical evaluation of the brains, which revealed widespread apoptotic neuronal death and increased levels of protein carbonyls. Furthermore, we detected changes in proteins involved in synaptic function, cell proliferation and formation of neuronal connections, suggesting interference of oxidative stress with these developmental events. These effects are age-dependent, as they did not occur in mice subjected to hyperoxia in adolescence.Cell Death and Differentiation (2006) 13, 1097–1109. doi:10.1038/sj.cdd.4401796; published online 28 October 2005 [ABSTRACT FROM AUTHOR]

Published
2006
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44. The basal ganglia, the deep prepyriform cortex, and seizure spread: bicuculline is anticonvulsant in the rat striatum.

Author

Turski, L, Cavalheiro, E A, Calderazzo-Filho, L S, Bortolotto, Z A, Klockgether, T, Ikonomidou, C, and Turski, W A

Abstract

The gamma-aminobutyric acid antagonist, bicuculline methiodide (BMI), induces myoclonic seizures in rats when injected into the deep prepyriform cortex at concentrations lower than those that induce convulsions from the amygdala, hippocampus, or neocortex. This observation prompted the suggestion that the deep prepyriform cortex was responsible for seizure generation regardless of the neurotransmitter and neuronal circuits involved. Bilateral intrastriatal application of BMI protects rats against seizures induced by (i) local application of BMI into the deep prepyriform cortex and (ii) systemic application of bicuculline, pilocarpine (a cholinergic agonist), or kainic acid (a glutamate receptor agonist). The region of the striatum sensitive to the previously unknown anticonvulsant action of BMI is located in the immediate vicinity of the deep prepyriform cortex and is 100-150 times more sensitive to the anticonvulsant action relative to the sensitivity of the deep prepyriform cortex to the convulsant action of BMI. These data suggest a powerful gamma-aminobutyric acid-dependent gating role of the basal ganglia in determining the seizure threshold in the forebrain. This argues against the suggestion that the deep prepyriform cortex plays a crucial role in the generation of seizures following systemic administration of convulsants. The discovery of an anticonvulsant action of BMI in the rat striatum contradicts the gamma-aminobutyric acid theory of epilepsy, which implies that deficits in the gamma-aminobutyric acid-mediated inhibition in the central nervous system lead to the emergence of seizures.

Published
1989
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