“…This neuron-like morphology is similar to that described by others [Clagett-Dame et al, 2006;Cheung et al, 2009]. Moreover, the in vitro reconstruction of the neuronal network obtained in this work on PCL membranes clearly indicates the neuronal differentiation, which is in ac- Bartolo et al, 2008;Morelli et al, 2010Morelli et al, , 2012b. To confirm that the observed morphological features were actually resulting from the neuronal differentiation of SH-SY5Y cells, the expression of specific neuronal markers, βIII-tubulin and synaptophysin, were investigated by immunocytochemical analysis.…”
Section: Discussionmentioning
confidence: 64%
“…The present study investigates the protective effect of didymin against H 2 O 2 -induced damage to the neuronal cells in a biohybrid membrane system model. Previous studies have demonstrated that semipermeable polymeric membranes in flat and hollow fiber configurations, thanks to their highly selective structural, physicochemical and transport properties, allow the successful in vitro reconstruction of neuronal tissue, reproducing a tissue model for studying metabolic diseases and drug effects [Woerly et al, 1996;Schmidt and Leach, 2003;Zhang et al, 2005;De Bartolo et al, 2008;Giusi et al, 2009;He et al, 2009;Morelli et al, 2010;Di Vito et al, 2011;Morelli et al, 2012b, c]. It was recently reported that polycaprolactone (PCL)-based membranes successfully supported outgrowth and differentiation of human neuronal cells [Morelli et al, 2012a].…”
In this study, the flavonoid didymin was administered in vitro in neuronal cells after hydrogen peroxide (H2O2)-induced injury (neurorescue) in order to investigate the effects of this natural molecule on cell damage in a neuronal membrane system. The results showed the effects of didymin in neuronal cells by using a polycaprolactone biodegradable membrane system as an in vitro model. Two major findings are presented in this study: first is the antioxidant property of didymin and, second, for the first time we provide evidence concerning its ability to rescue neuronal cells from oxidative damage. Didymin showed radical scavenging activities and it protected the neuronal cells against H2O2-induced neurotoxicity. Didymin increased cell viability, decreased intracellular reactive oxygen species generation, stimulated superoxide dismutase, catalase and glutathione peroxidase activity in neuronal cells which were previously insulted with H2O2. In addition, didymin strikingly inhibited H2O2-induced mitochondrial dysfunctions in terms of reduction of mitochondria membrane potential and the activation of cleaved caspase-3, and also decreased dramatically the H2O2-induced phosphorylation of c-Jun N-terminal kinase. Therefore, this molecule is capable of inducing recovery from oxidative damage, and promoting and/or restoring normal cellular conditions. Moreover, the mechanism underlying the protective effects of didymin in H2O2-injured neuronal cells might be related to the activation of antioxidant defense enzymes as well as to the inhibition of apoptotic features, such as p-JNK and caspase-3 activation. These data suggest that didymin may be a potential therapeutic molecule for the treatment of neurodegenerative disorders associated with oxidative stress.
“…This neuron-like morphology is similar to that described by others [Clagett-Dame et al, 2006;Cheung et al, 2009]. Moreover, the in vitro reconstruction of the neuronal network obtained in this work on PCL membranes clearly indicates the neuronal differentiation, which is in ac- Bartolo et al, 2008;Morelli et al, 2010Morelli et al, , 2012b. To confirm that the observed morphological features were actually resulting from the neuronal differentiation of SH-SY5Y cells, the expression of specific neuronal markers, βIII-tubulin and synaptophysin, were investigated by immunocytochemical analysis.…”
Section: Discussionmentioning
confidence: 64%
“…The present study investigates the protective effect of didymin against H 2 O 2 -induced damage to the neuronal cells in a biohybrid membrane system model. Previous studies have demonstrated that semipermeable polymeric membranes in flat and hollow fiber configurations, thanks to their highly selective structural, physicochemical and transport properties, allow the successful in vitro reconstruction of neuronal tissue, reproducing a tissue model for studying metabolic diseases and drug effects [Woerly et al, 1996;Schmidt and Leach, 2003;Zhang et al, 2005;De Bartolo et al, 2008;Giusi et al, 2009;He et al, 2009;Morelli et al, 2010;Di Vito et al, 2011;Morelli et al, 2012b, c]. It was recently reported that polycaprolactone (PCL)-based membranes successfully supported outgrowth and differentiation of human neuronal cells [Morelli et al, 2012a].…”
In this study, the flavonoid didymin was administered in vitro in neuronal cells after hydrogen peroxide (H2O2)-induced injury (neurorescue) in order to investigate the effects of this natural molecule on cell damage in a neuronal membrane system. The results showed the effects of didymin in neuronal cells by using a polycaprolactone biodegradable membrane system as an in vitro model. Two major findings are presented in this study: first is the antioxidant property of didymin and, second, for the first time we provide evidence concerning its ability to rescue neuronal cells from oxidative damage. Didymin showed radical scavenging activities and it protected the neuronal cells against H2O2-induced neurotoxicity. Didymin increased cell viability, decreased intracellular reactive oxygen species generation, stimulated superoxide dismutase, catalase and glutathione peroxidase activity in neuronal cells which were previously insulted with H2O2. In addition, didymin strikingly inhibited H2O2-induced mitochondrial dysfunctions in terms of reduction of mitochondria membrane potential and the activation of cleaved caspase-3, and also decreased dramatically the H2O2-induced phosphorylation of c-Jun N-terminal kinase. Therefore, this molecule is capable of inducing recovery from oxidative damage, and promoting and/or restoring normal cellular conditions. Moreover, the mechanism underlying the protective effects of didymin in H2O2-injured neuronal cells might be related to the activation of antioxidant defense enzymes as well as to the inhibition of apoptotic features, such as p-JNK and caspase-3 activation. These data suggest that didymin may be a potential therapeutic molecule for the treatment of neurodegenerative disorders associated with oxidative stress.
“…Other studies have investigated neuronal guidance potential of microgrooves in similar dimensions of a few lm-range, for example on PC-12 cells on poly(lactide-co-glycolide) (PLGA) 21 and on copolymer 2-norbornene ethylene [cyclic olefin copolymer (COC)] foils 31 or primary hippocampal neurons on poly(L-lactic acid) (PLLA). 40 Bigger groove dimensions seem to be ineffective for neurite alignment of astrocytes 27 but not of dorsal root ganglion cells. 41 In addition to the alignment, the influence of surface topography on neurite length was investigated.…”
CitationDirecting neuronal cell growth on implant material surfaces by microstructuring. 2012, 100 (4) Abstract: For best hearing sensation, electrodes of auditory prosthesis must have an optimal electrical contact to the respective neuronal cells. To improve the electrode-nerve interface, microstructuring of implant surfaces could guide neuronal cells toward the electrode contact. To this end, femtosecond laser ablation was used to generate linear microgrooves on the two currently relevant cochlear implant materials, silicone elastomer and platinum. Silicone surfaces were structured by two different methods, either directly, by laser ablation or indirectly, by imprinting using laser-microstructured molds. The influence of surface structuring on neurite outgrowth was investigated utilizing a neuronal-like cell line and primary auditory neurons. The pheochromocytoma cell line PC-12 and primary spiral ganglion cells were cultured on microstructured auditory implant materials. The orientation of neurite outgrowth relative to the microgrooves was determined. Both cell types showed a preferred orientation in parallel to the microstructures on both, platinum and on molded silicone elastomer. Interestingly, microstructures generated by direct laser ablation of silicone did not influence the orientation of either cell type. This shows that differences in the manufacturing procedures can affect the ability of microstructured implant surfaces to guide the growth of neurites. This is of particular importance for clinical applications, since the molding technique represents a reproducible, economic, and commercially feasible manufacturing procedure for the microstructured silicone surfaces of medical implants. V C 2012 Wiley Periodicals, Inc.J Biomed Mater Res Part B: Appl Biomater 00B: 000-000, 2012.
“…Diffusible [1] and surface bound molecule gradients [2], [3], [4], chemical surface patterning [5], [6] or mechanical structures like pillars [7], micromachined steps, ridges or groove gratings at the (sub-)micrometer scale are promising as guidance cues [8], [9], [10], [11], [12], [13], [14], [15].…”
The treatment of critical size peripheral nerve defects represents one of the most serious problems in neurosurgery. If the gap size exceeds a certain limit, healing can't be achieved. Connection mismatching may further reduce the clinical success. The present study investigates how far specific surface structures support neurite outgrowth and by that may represent one possibility to push distance limits that can be bridged. For this purpose, growth cone displacement of fluorescent embryonic chicken spinal cord neurons was monitored using time-lapse video. In a first series of experiments, parallel patterns of polyimide ridges of different geometry were created on planar silicon oxide surfaces. These channel-like structures were evaluated with and without amorphous hydrogenated carbon (a-C:H) coating. In a next step, structured and unstructured textile fibers were investigated. All planar surface materials (polyimide, silicon oxide and a-C:H) proved to be biocompatible, i.e. had no adverse effect on nerve cultures and supported neurite outgrowth. Mean growth cone migration velocity measured on 5 minute base was marginally affected by surface structuring. However, surface structure variability, i.e. ridge height, width and inter-ridge spacing, significantly enhanced the resulting net velocity by guiding the growth cone movement. Ridge height and inter-ridge distance affected the frequency of neurites crossing over ridges. Of the evaluated dimensions ridge height, width, and inter-ridge distance of respectively 3, 10, and 10 µm maximally supported net axon growth. Comparable artificial grooves, fabricated onto the surface of PET fibers by using an excimer laser, showed similar positive effects. Our data may help to further optimize surface characteristics of artificial nerve conduits and bioelectronic interfaces.
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