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At least 37 records · Page 2Linked to original sources
PubMed1999

Tumor cell viability in clear cell sarcoma requires DNA binding activity of the EWS/ATF1 fusion protein.

Chimeric proteins resulting from characteristic chromosomal translocations are believed to play a key role in the development of neoplasia. The consistent chromosomal translocation t(12;22) found in Clear Cell sarcoma (CCS) fuses the genes for Ewing's sarcoma protein (EWS) and activating transcription factor 1 (ATF1). Contribution of the chimeric EWS/ATF1 protein to maintenance of the tumor phenotype was investigated using intracellular expression of an inhibitory anti-ATF1 single chain antibody fragment (scFv4). Transfection of scFv4 into a cell line (SU-CCS-1) derived from CCS resulted in a 90% reduction in cyclic AMP response element-driven reporter activity. The delivery of scFv4 into SU-CCS-1 cells by a Moloney sarcoma retroviral vector (SRalpha-Fv4) significantly reduced viability and induced apoptosis as measured by terminal deoxynucleotidetransferase-mediated dUTP-biotin nick end labeling and flow cytometry. Conversely, scFv4 had no effect on viability of HeLa cells. The level of EWS/ATF1 expression was found to be significantly higher in primary tumor tissue than in SU-CCS-1 cells or in 293T cells following introduction of an EWS/ATF1 expression vector. These studies demonstrate a direct role for the EWS/ATF1 fusion protein in maintaining tumor cell viability of Clear Cell sarcoma and indicate that intracellular antibodies may be used to achieve a phenotypic knockout of tumor-related proteins as a method to explore their function.

Apoptosis↗
PubMed1998

Reduced DNA synthesis and cell viability in small cell lung carcinoma by treatment with cyclic AMP phosphodiesterase inhibitors.

This study investigated the effects of the adenosine 3',5'-cyclic monophosphate (cAMP) phosphodiesterase inhibitors caffeine, theophylline, and 3-isobutyl-1-methyl-xanthine (IBMX) on the proliferation and viability of the small cell lung carcinoma (SCLC) cell lines NCI-H345, NCI-H128, and SCC-9. These effects were correlated with the ability of the drugs to induce intracellular Ca2+ mobilization. Treatment of NCI-H345 cells with caffeine resulted in rapid mobilization of Ca2+, as indicated by Fura-2 fluorescence. Incubation of NCI-H345 cells with 6.25 mM caffeine resulted in a 62% inhibition of [3H]thymidine uptake after 2 hr, indicating reduced DNA synthesis. Incubation with 25 mM caffeine resulted in almost total inhibition of [3H]thymidine uptake after 2 hr. Similar effects on [3H]thymidine uptake were seen upon treatment of NCI-H128 and SCC-9 cells with caffeine; however, these cells did not exhibit caffeine-induced Ca2+ mobilization. Inhibition of DNA synthesis (66-93%) also occurred upon incubation of all cell lines with theophylline and IBMX, which did not mobilize Ca2+. Treatment of NCI-H345, NCI-H128, and SCC-9 cells with caffeine, theophylline, or IBMX markedly reduced cell viability. Levels of cAMP increased in the cells following treatment with caffeine, theophylline, or IBMX, reflecting the ability of these drugs to inhibit cAMP phosphodiesterase. These results suggest that the decrease in DNA synthesis and the subsequent cell death induced by these drugs are due to reduced cAMP phosphodiesterase activity, rather than to changes in intracellular Ca2+. These findings indicate that drugs that alter cAMP signaling pathways are potentially valuable agents to inhibit SCLC survival.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1994

An alternative method for obtaining high-viability cell suspensions from neonatal mouse brain.

Cultured brain cells have contributed greatly to our understanding of a variety of neurobiological processes. The ability to culture brain tissue is important for studying cellular processes underlying unique neural properties. Traditional culturing techniques commonly involve triturating tissue through glass Pastuer pipets, which are inappropriate for use with potentially biohazardous materials. We therefore developed an alternative method for dissociating brain tissue. The protocol combines enzymatic digestion and mechanical dissociation with additives to the dissection medium that protect the cells against other sources of injury, including glutamate neurotoxicity, oxidative damage, and excessively alkaline pH. We find this method works well with post-natal mouse brain, consistently giving cell viabilities in the range of 92-99% and an average yield of 3.1 x 10(6) cells per mouse.

Animals↗
PubMed1986

Biphasic effects of chlorpromazine on cell viability in a neuroblastoma cell line.

Although chlorpromazine was shown to greatly inhibit a Ca2+-mediated cell death at favorable concentrations (10(-6)-10(-5) M), it caused a drastic decrease in cell viability at higher concentrations (10(-4)-10(-3) M) in a human neuroblastoma cell line. The toxic effect of chlorpromazine also occurred in Ca2+-free medium and was not parallel to the amount of thiobarbituric acid-reactive substances produced. These results indicate that chlorpromazine has biphasic effects on cell viability according to the concentrations added, i.e. a protective effect against cell damage caused by Ca2+, and a direct toxic effect independent of extracellular Ca2+ or of lipid peroxidation.

Calcium↗
PubMed1997

Cell viability and probe-cell membrane interactions of XR1 glial cells imaged by atomic force microscopy.

As atomic force microscopy (AFM) imaging of live specimens becomes more commonplace, at least two important questions arise: 1) do live specimens remain viable during and after AFM, and 2) is there transfer of membrane components from the cell to the AFM probe during probe-membrane interactions? We imaged live XR1 glial cells in culture by single- or dual-pass contact or tapping-mode AFM, examined cell viability at various postimaging times, and report that AFM-imaged live XR1 cells remained viable up to 48 h postimaging and that cell death rates did not increase. To determine if nonlethal, transient interactions between the AFM probe and cell membrane led to transfer of XR1 cell membrane phospholipid components on the probe, we treated the scanned probes with the lipid-binding fluorophore FM 1-43. Confocal microscopy revealed that phospholipid membrane components did accumulate on the probe, and to a generally greater extent during contact-mode imaging than during tapping-mode imaging. Moreover, membrane accumulations on the probe were greater when live XR1 cells were damaged or perturbed, yet membrane did not accumulate in fluorescently detectable quantities during repeated "force curves" during control experiments. Taken together, our data indicate that although AFM imaging of live cells in culture does not affect long-term cell viability, there are substantial probe-membrane interactions that lead to transfer of membrane components to the probe.

Animals↗
PubMed2006

Tumor necrosis factor-alpha regulates steroidogenesis, apoptosis, and cell viability in the human adrenocortical cell line NCI-H295R.

TNF-alpha regulates the hypothalamo-pituitary-adrenal axis at several levels. It has been shown to modify adrenal steroidogenesis in many species, and it is supposed to act as an auto/paracrine factor. However, its significance in human adrenocortical function remains unclear. Therefore, we investigated the effect of TNF-alpha on adrenal steroidogenesis, expression of the key steroidogenic genes, apoptosis, and cell viability in the human adrenocortical cell line NCI-H295R. TNF-alpha treatment (1 nM for 48 h) decreased the basal production of cortisol, androstenedione, dehydroepiandrosterone sulfate (DHEAS), and aldosterone (14, 18, 35, and 52%, respectively), and the 8-bromo-cAMP-induced production of cortisol, androstenedione, dehydroepiandrosterone (DHEA), and DHEAS (44, 66, 58, and 48%, respectively). However, when the steroid production data were normalized by the cell number, TNF-alpha increased the basal production of cortisol, androstenedione, DHEA, DHEAS, and aldosterone (137, 121, 165, 73, and 28%, respectively), and the 8-bromo-cAMP-induced production of cortisol, DHEAS, and aldosterone (122, 121, and 256%, respectively). This was accompanied by a parallel increase in the expression of the genes encoding for the steroidogenic acute regulatory protein, 3beta-hydroxysteroid dehydrogenase 2, and 17-hydroxylase/17,20-lyase (74, 200, and 50%, respectively; quantitative real-time RT-PCR analysis). TNF-alpha increased caspase 3/7 activity (an indicator of apoptosis) and decreased cell viability dose and time dependently. The effect of TNF-alpha on apoptosis was neutralized by a monoclonal TNF-alpha antibody. These findings indicate that TNF-alpha is a potent regulator of steroidogenesis and cell viability in adrenocortical cells. TNF-alpha may have physiological and/or pathophysiological significance as an endocrine and/or paracrine/autocrine regulator of adrenocortical function.

3-Hydroxysteroid Dehydrogenases↗
PubMed2001

Effects of uwhangchungsimwon on cell viability, proliferation, and gene expression of human neuronal cell line IMR32.

Uwhangchungsimwon (pill, UC) is one of the traditional Korean medical prescriptions that has been most frequently used for stroke. To characterize the effects of UC on human neuronal cells, the human neuroblastoma cell line IMR32 was treated with UC, and cell viability, cell proliferation, apoptosis, and gene expression were analyzed. The effect of UC on recovery of cell viability was analyzed following stress induction by nutrient depletion or cold shock. Flow cytometric analysis of the cell cycle showed that UC inhibits cell cycle progression of IMR32 in a dose- and time-dependent manner. UC was also identified to increase cell viability and suppress apoptosis induction by a DNA-damaging agent, etoposide. Quantitative RT-PCR analysis revealed that expressions of the p53 tumor suppressor gene and its downstream effect, Waf1, are stimulated whereas expressions of positive cell cycle regulators, c-Myc, c-Fos, and Cyclin D1 were repressed by UC treatment. Moreover, while expression levels of apoptosis inhibitors, Bcl-2 and Bcl-XL were increased following UC treatment, that of an apoptosis promoter, Bax, was decreased. In addition, expression of BMP-7, which has been recently demonstrated to improve the motor neuron recovery from stroke, was induced by UC while it was not detected in untreated cells. Taken together, our data suggest that the pharmacoclinical effects of UC might be derived in part from its negative regulation of cell proliferation and apoptosis through the transcriptional control of related genes.

Apoptosis↗
PubMed2002

The effects of particulate metals on cell viability of osteoblast-like cells in vitro.

Effects of fifteen particulate objects, fourteen metals and one non-metal on cell viability of osteoblast-like cells were studied in vitro, to determine whether an adverse effect on cells could be induced by the particulate form or soluble ions. The Al, Ti, Zr, Nb, Ta, Cr, Mo, and Fe particulates depressed cell viability at higher particulate concentrations, but their extracts yielded no effect on cells except for Mo. On the other hand, little difference in cell viability between particulates and extracts was observed for Cu, Si, V, W, and Co. However, Mn and Ni yielded more adverse effects on cells in the case of the particulates than the extracts. These findings suggested that the effects of particulates on cells depended upon the direct effects of contact between particulates and cells, the indirect effects of dissolved ions and the kinds of particulate elements.

Aluminum↗
PubMed2006

Differential protective effects of palmitoleic acid and cAMP on caspase activation and cell viability in pancreatic beta-cells exposed to palmitate.

Saturated and mono-unsaturated fatty acids exert differential effects on pancreatic beta-cell viability during chronic exposure. Long chain saturated molecules (e.g. palmitate) are cytotoxic to beta-cells and this is associated with caspase activation and induction of apoptosis. By contrast, mono-unsaturated fatty acids (e.g. palmitoleate) are not toxic and can protect against the detrimental effects of palmitate. In the present study, we show that the protective actions of palmitoleate in BRIN-BD11 beta-cells result in attenuated caspase activation following exposure to palmitate and that a similar response occurs in cells having elevated levels of cAMP. However, unlike palmitoleate, elevation of cAMP was unable to prevent the cytotoxic actions of palmitate since it caused a diversion of the pathway of cell death from apoptosis to necrosis. Palmitoleate did not alter cAMP levels in BRIN-BD11 cells and the results suggest that a change in cAMP is not involved in mediating the protective effects of this fatty acid. Moreover, they reveal that attenuated caspase activation does not always correlate with altered cell viability in cultured beta-cells and suggest that mono-unsaturated fatty acids control cell viability by regulating a different step in the apoptotic pathway from that influenced by cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed1997

A system for simultaneous evaluation of the effect of signal transduction inhibitors on interleukin-2 synthesis and cell viability in a human T cell line.

BACKGROUND: The signal transduction pathways involved in interleukin-2 (IL-2) synthesis have become a focus of interest for pharmacological intervention. Regulation of synthesis of IL-2 requires costimulation of two cell surface receptors, the T cell receptor and an appropriate costimulatory receptor. Antibodies such as anti-CD3 to stimulate the T cell receptor and anti-CD28 can be used to induce this costimulation. Previous methodologies employed antibody coupled to polystyrene microtiter plates or solution phase stimulation. METHODS: Here, a method using magnetic beads to present anti-CD3 and anti-CD28, to the Jurkat T cell line was developed. Conditions were also developed for simultaneous analysis of the effect of test compounds on cell viability. The IL-2 synthesis methods and cell viability methods have been used to evaluate signal transduction inhibitors. RESULTS: This method was then employed to test the effects of various signal transduction inhibitors on IL-2 synthesis. Agents which increase cAMP, cyclosporin and inhibitors of calmodulin, tyrosine kinases/phosphatases, protein kinase C, and PC-PL-C decrease IL-2 synthesis at concentrations which do not affect cell viability. CONCLUSION: These results found with this novel system of stimulation with antibody to CD3 and CD28 compare favorably with activities reported in the literature thus validating this rapid facile system for evaluation of the effect of signal transduction inhibitors in IL-2 synthesis.

Antibodies↗
PubMed2002

Differential effect of catecholamines and MPP(+) on membrane permeability in brain mitochondria and cell viability in PC12 cells.

The present study examined the effect of dopamine, 6-hydroxydopamine (6-OHDA), and MPP(+) on the membrane permeability transition in brain mitochondria and on viability in PC12 cells. Dopamine and 6-hydroxydopamine induced the swelling and membrane potential change in mitochondria, which was inhibited by addition of antioxidant enzymes, SOD and catalase. In contrast, antioxidant enzymes did not reduce the effect of MPP(+) on mitochondrial swelling and membrane potential. Catecholamines enhanced the Ca(2+) uptake and release by mitochondria, and the addition of MPP(+) induced Ca(2+) release. Catecholamines induced a thiol oxidation in mitochondria that was decreased by antioxidant enzymes. MPP(+) showed a little effect on the cytochrome c release from mitochondria and did not induce thiol oxidation. Catecholamines and MPP(+) induced a cell death, including apoptosis, in PC12 cells that was inhibited by addition of antioxidant enzymes. The result suggests that the oxidation of dopamine and 6-hydroxydopamine could modulate the membrane permeability in brain mitochondria and induce PC12 cell death, which may be ascribed to oxidative stress. MPP(+) appears to exert a toxic effect on neuronal cells by the action, which is different from catecholamines.

1-Methyl-4-phenylpyridinium↗
PubMedDate not supplied

Predictive value of intracellular ATP level for cell viability after heating in malignant cells.

An adenosine triphosphate (ATP) assay is known to be a useful chemosensitivity test, which correctly reflects cell viability. We investigated the usefulness of ATP assay as a thermosensitivity test by comparing two world-wide accepted assays which included a succinate dehydrogenase (SD) assay and a colony assay. We exposed KSE-1 and KSE-2 cell lines to various degrees of hyperthermia at 42, 43 and 44 degrees C for 0.5, 1, 2, 3 and 4 h, respectively. The ATP activity for the KSE-1 and KSE-2 cell lines was 2.0 and 0.7% in change of cell viability after heating at 44 degrees C for 4 h, respectively. Colony formation rates in the KSE-1 and KSE-2 cell lines were 0.9 and 0%, respectively, whereas the SD activity of each cell line was 24.1 and 22.8%. As a whole, the ATP assay showed a closer correlation to the colony assay than the SD assay because the latter revealed a more than 20% pseudo-viability due to the response between the base and residual enzyme even after the cells had died. Thus, the ATP assay was judged to be more sensitive than the SD assay; it was also quicker than the colony assay in evaluating cell viability after heating. We propose that the ATP assay should be included as another useful thermosensitivity test for malignant cells.

Adenosine Triphosphate↗
PubMed2001

Intracellular drug delivery using low-frequency ultrasound: quantification of molecular uptake and cell viability.

PURPOSE: To determine the dependence on acoustic parameters of molecular uptake and viability of cells exposed to low-frequency ultrasound. METHODS: DU145 prostate cancer cells bathed in a solution of calcein were exposed to ultrasound at 24 kHz over a range of different acoustic pressures. exposure times, pulse lengths, and duty cycles. Flow cytometry was employed to quantify the number of calcein molecules delivered into each cell and levels of cell viability. RESULTS: Both molecular uptake and cell viability showed a strong dependence on acoustic pressure and exposure time, weak dependence on pulse length, and no significant dependence on duty cycle. When all of the data were pooled together, they exhibited good correlation with acoustic energy exposure. Although molecular uptake showed large cell-to-cell heterogeneity, up to approximately 15% of cells achieved an intracellular calcein concentration approximately equal to its extracellular concentration. CONCLUSIONS: Large numbers of molecules can be delivered intracellularly using low-frequency ultrasound. Both uptake and viability correlate with acoustic energy, which is useful for design and control of ultrasound protocols.

Cell Membrane↗
PubMed2000

Inhibition of tyrosinase reduces cell viability in catecholaminergic neuronal cells.

The biosynthesis of dopamine (DA) in catecholaminergic neurons is regulated by tyrosine hydroxylase, which converts tyrosine into 3, 4-dihydroxyphenylalanine (L-DOPA). In melanocytes, tyrosinase catalyzes both the hydroxylation of tyrosine and the consequent oxidation of L-DOPA to form melanin. Although it has been demonstrated that tyrosinase is also expressed in the brain, the physiological role of tyrosinase in the brain is still obscure. In this study, to investigate the role of tyrosinase in catecholaminergic neuronal cells, we examined the effects of tyrosinase inhibition on the viability of CATH.a and SH-SY5Y cells using tyrosinase inhibitors-specifically, phenylthiourea (PTU) and 5-hydroxyindole (5-HI)-and the transfection of antisense tyrosinase cDNA. Both inhibitors significantly reduced the cell viability of CATH.a cells in a dose-dependent manner. PTU also specifically enhanced DA-induced cell death, but 5-HI did not. This discrepancy in cell death is probably due to the inhibitors' different mechanism of action: 5-HI inhibits the hydroxylation of tyrosine as a competitor for the substrate to induce cell death that may be due to depletion of DA, whereas PTU mainly inhibits the enzymatic oxidation of L-DOPA and DA rather than tyrosine hydroxylation to increase consequently autooxidation of DA. Indeed, the intracellular DA content in CATH.a cells was enhanced by PTU exposure. In contrast, PTU showed no enhancing effects on DA-induced cell death of SH-SY5Y cells, which express little tyrosinase. Furthermore, transfection with antisense tyrosinase cDNA into CATH.a cells dramatically reduced cell viability and significantly enhanced DA-induced cell death. These results suggest that tyrosinase controls the intracellular DA content by biosynthesis or enzymatic oxidation of DA, and the dysfunction of this activity induces cell death by elevation of intracellular DA level and consequent gradual autooxidation of DA to generate reactive oxygen species.

Animals↗
PubMed2004

Protective effect of 1-methylated beta-carbolines against 3-morpholinosydnonimine-induced mitochondrial damage and cell viability loss in PC12 cells.

The present study investigated the effect of 1-methylated beta-carbolines (harmaline, harmalol and harmine) on change in the mitochondrial membrane permeability and cell death due to reactive nitrogen species in differentiated PC12 cells. beta-Carbolines, caspase inhibitors (z-LEHD.fmk and z-DQMD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol, melatonin, carboxy-PTIO and uric acid) depressed cell viability loss due to 3-morpholinosydnonimine (SIN-1) in PC12 cells. beta-Carbolines inhibited the nuclear damage, the decrease in mitochondrial transmembrane potential, the cytochrome c release, the formation of reactive oxygen species and the depletion of GSH caused by SIN-1 in PC12 cells. beta-Carbolines decreased the SIN-1-induced formations of 3-nitrotyrosine, malondialdehyde and carbonyls in PC12 cells. The results show that 1-methylated beta-carbolines attenuate SIN-1-induced mitochondrial damage. This results in the inhibition of caspase-9 and -3 and apoptotic cell death in PC12 cells by suppressing the toxic actions of reactive oxygen and nitrogen species, including the GSH depletion.

Animals↗
PubMed2005

Effects of tocotrienols on cell viability and apoptosis in normal murine liver cells (BNL CL.2) and liver cancer cells (BNL 1ME A.7R.1), in vitro.

The effects of tocotrienols on murine liver cell viability and their apoptotic events were studied over a dose range of 0-32 microg mL(-1). Normal murine liver cells (BNL CL.2) and murine liver cancer cells (BNL 1ME A.7R.1) were treated with tocotrienols (T(3)), alpha tocopherol (alpha-T) and the chemo drug, Doxorubicin (Doxo, as a positive control). Cell viability assay showed that T(3) significantly (P < or = 0.05) lowered the percentage of BNL 1ME A.7R.1 cell viability in a dose-responsive manner (8-16 microg mL(-1)), whereas T did not show any significant (P>0.05) inhibition in cell viability with increasing treatment doses of 0-16 microg mL(-1). The IC(50) for tocotrienols were 9.8, 8.9, 8.1, 9.7, 8.1 and 9.3 microg mL(-1) at 12, 24, 36, 48, 60 and 72 hours respectively. Early apoptosis was detected 6 hours following T(3) treatment of BNL 1ME A.7R.1 liver cancer cells, using Annexin V-FITC fluorescence microscopy assay for apoptosis, but none were observed for the non-treated liver cancer cells at the average IC(50) of 8.98 microg mL(-1) tocotrienols for liver cancer cells. Several apoptotic bodies were detected in BNL 1ME A.7R.1 liver cancer cells at 6 hours post-treatment with tocotrienols (8.98 microg mL(-1)) using Acridine Orange/Propidium Iodide fluorescence assay. However, only a couple of apoptotic bodies were seen in the non-treated liver cancer cells and the BNL CL.2 normal liver cells. Some mitotic bodies were also observed in the T(3)-treated BNL 1ME A.7R.1 liver cancer cells but were not seen in the untreated BNL 1ME A.7R.1 cells and the BNL CL.2 liver cells. Following T(3)-treatment (8.98 microg mL(-1)) of the BNL 1ME A.7R.1 liver cancer cells, 24.62%, 25.53% and 44.90% of the cells showed elevated active caspase 3 activity at 9, 12 and 24 hours treatment period, respectively. DNA laddering studies indicated DNA fragmentation occurred in the T(3)-treated liver cancer cells, BNL 1ME A.7R.1 but not in non-treated liver cancer cells and the T(3)-treated and non-treated normal liver cells. These results suggest that tocotrienols were able to reduce the cell viability in the murine liver cancer cells at a dose of 8-32 microg mL(-1) and that this decrease in percentage cell viability may be due to apoptosis.

Animals↗
PubMed1987

The effect of automobile exhaust particulates on cell viability, plating efficiency and cell division of mammalian tissue culture cells.

Extract of particulate matter (EPM) of gasoline engine exhaust induced only a slight loss of cell viability of mouse macrophages (line IC-21) in vitro, while a strong dose-dependent reduction of plating efficiency of human cell line A-549 and of Syrian hamster line 14-1b occurred. Cytological investigations of exposed macrophages of line IC-21 revealed an increase in the mitotic index from 1.5% of control values up to 14.6% at the highest tested concentration of EPM. Mitotic arrest is based almost exclusively on C-type mitoses occurring dose-dependently in the presence of EPM. Results indicate disturbances of the spindle apparatus in the presence of EPM.

Animals↗
PubMed2006

Differential cell viability of chondrocytes and progenitor cells in tissue-engineered constructs following implantation into osteochondral defects.

Animal studies in cartilage tissue engineering usually include the transfer of cultured cells into chondral or osteochondral defects. Immediately at implantation, the cells are exposed to a dramatically changed environment. The aim of this study was to determine the viability of two cell types currently considered for cellular therapies of cartilage defects-chondrocytes and progenitor cells-shortly after exposure to an osteochondral defect in rabbit knees. To that end, autogenic chondrocytes and periosteal cells were labeled with CM-DiI fluorochrome, seeded or cultured in PEGT/PBT scaffolds for periods up to 2 weeks, transferred into osteochondral defects, harvested 5 days postimplantation, and analyzed for cell viability. In order to further elucidate factors effecting cell viability within our model system, we investigated the effect of serum, 2) extracellular matrix surrounding implanted cells, 3) scaffold interconnectivity, and 4) hyaluronan, as a known cell protectant. Controls included scaffolds with devitalized cells and scaffolds analyzed at implantation. We found that the viability of periosteum cells (14%), but not of chondrocytes (65-95%), was significantly decreased after implantation. The addition of hyaluronan increased periostium cell viability to 44% (p < 0.05). Surprisingly, cell viability in less interconnected compression-molded scaffolds was higher compared to that of fully interconnected scaffolds produced by rapid prototyping. All other factors tested did not affect viability significantly. Our data suggest chondrocytes as a suitable cell source for cartilage repair in line with clinical data on several chondrocyte-based therapies. Although we did not test progenitor cells other the periosteum cells, tissue-engineering approaches using such cell types should take cell viability aspects into consideration.

Animals↗