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Abstract
Fullerenes are carbon nanoparticles with the ability to quench reactive oxygen species. The biomedical potential of fullerenes is diminished by their low solubility in water, but many approaches have been developed to bypass this problem, like chemical modification of the carbon cage and the use of the solvent exchange method to transfer fullerenes from one solvent to the other. These two approaches were used in this study. Carboxylated fullerene aqueous solution was acquired using solvent exchange method transferring fullerene nanoparticles (C60) from toluene to water. Effects of varying concentration (0.5, 1, 1.5, 2, 2.5, 3, 5, 10 µM) of aqueous fullerene solution on cell viability and their antioxidative capabilities were evaluated on PC-3 and on monocytes isolated from a blood donor using Resazurin Cell Viability Assay. PC-3 cell viability was drastically affected by the 10 µM fullerene solution but remained relatively stable when treated with other concentrations even after longer periods of incubation with resazurin dye. Elevated cell viability was observed in monocytes treated with various fullerene concentrations, possibly indicative of fullerene protective activity against oxidative stress.

Purpose To investigate the effects of methylene blue (MB) on the viability and secretory phenotype of rat nucleus pulposus (NP) cells in vitro.
Methods Rat NP cells were isolated, cultured, and treated with different MB concentrations (0–6.25 ng/mL) for different lengths of time. We evaluated the changes in cell morphology and cell viability. We also examined the cells for expression of collagen II, aggrecan, matrix metalloproteinase (MMP)-3, MMP-9, and inducible nitric oxide synthase (iNOS).
Results After 2.5 to 6.25 ng/mL MB induced for 6 hours, numerous NP cells were dyed blue and rounded up. The adherent cell number was reduced by MB treatment. The viability of rat NP cells was significantly inhibited by MB in a dose- and time-dependent manner. Treatment with a very low dose of MB (1.5625 ng/mL) resulted in lower expression of collagen II and aggrecan and higher expression of MMP-3, MMP-9, and iNOS in rat NP cells.
Conclusions Rat NP cells exposed in vitro to MB significantly reduced their viability. Moreover, MB upregulated catabolism gene expression and downregulated anabolism gene expression in rat NP cells. These results suggest MB may be harmful to NP cells. The dose of intradiskal injected MB should be as low as possible to prevent or limit the damage to intervertebral disks.

This is an Accepted Manuscript of an article published by Taylor & Francis in islets on 1 March 2013, available online: http://www.tandfonline.com/10.4161/isl.24249 ; Open Access article ; Pro-inflammatory cytokines are important mediators of β-cell demise in type 1 diabetes, and similar mechanisms are increasingly implicated in type 2 diabetes, where a state of chronic inflammation may persist. It is likely that the actions of anti-inflammatory cytokines are also altered in diabetes. Cytokines are released from immune cells, which may be recruited to the islets in diabetes, but they can also be produced by islet endocrine cells in response to environmental factors, including enteroviral infection. Since enteroviral infection of islet cells may influence the development of diabetes in humans, we examined the actions of two cytokines, IL-13 and IL-6, whose expression are reported to be altered in β-cells during enteroviral infection. Human and rodent islet cells were shown to express receptors for both IL-13 and IL-6, and treatment with either cytokine resulted in the rapid phosphorylation of STAT3 and STAT6. However, while β-cells were protected against a range of cytotoxic insults during exposure to IL-13, treatment with IL-6 enhanced cytotoxicity and western blotting revealed that IL-13 induced one specific isoform of phospho-STAT6 preferentially. Upon incubation with both cytokines together, the isoform of STAT6 that was upregulated by IL-13 alone was again induced, and the effects of IL-6 on β-cell viability were attenuated. Overall, the results suggest that induction of specific isoforms of STAT family transcription factors may underlie the cytoprotective actions of IL-13, and they imply that selective targeting of specific STAT-mediated signaling components could provide a means to ameliorate the loss of β-cell viability in diabetes. ; Nuffield Foundation - Bursary scheme ; European Union's Seventh Framework Programme PEVNET (FP7/2007-2013)

Temporo-mandibular joint disc disorders are highly prevalent in adult populations. Autologous chondrocyte implantation is a well-established method for the treatment of several chondral defects. However, very few studies have been carried out using human fibrous chondrocytes from the temporo-mandibular joint (TMJ). One of the main drawbacks associated to chondrocyte cell culture is the possibility that chondrocyte cells kept in culture tend to de-differentiate and to lose cell viability under in in-vitro conditions. In this work, we have isolated human temporo-mandibular joint fibrochondrocytes (TMJF) from human disc and we have used a highly-sensitive technique to determine cell viability, cell proliferation and gene expression of nine consecutive cell passages to determine the most appropriate cell passage for use in tissue engineering and future clinical use. Our results revealed that the most potentially viable and functional cell passages were P5–P6, in which an adequate equilibrium between cell viability and the capability to synthesize all major extracellular matrix components exists. The combined action of pro-apoptotic (TRAF5, PHLDA1) and anti-apoptotic genes (SON, HTT, FAIM2) may explain the differential cell viability levels that we found in this study. These results suggest that TMJF should be used at P5–P6 for cell therapy protocols. ; This work was supported by University of Granada-Campus de Excelencia Internacional, Subprograma de I+D+I y Transferencia and by the Spanish Ministry of Economy and Competitiveness, grant IPT-300000-2010-017 (INNPACTO program), co-financed by the European Regional Development Fund, European Union.