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PubMed2004

Extracellular ATP inhibits apoptosis and maintains cell viability by inducing autocrine production of interleukin-4 in a myeloid progenitor cell line.

Interleukin-3 (IL-3)-dependent myeloid progenitor cell FDC.P2 is induced to undergo apoptotic cell death upon IL-3 depletion. Extracellular adenosine triphosphate (ATP) was found to prevent apoptosis and maintain cell viability of FDC.P2 cells upon IL-3 withdrawal. The antiapoptotic effect of ATP required extracellular Ca2+. Furthermore, FK506, a specific inhibitor of calcium/calmodulin-dependent protein phosphatase calcineurin, inhibited the antiapoptotic effect of ATP. As one of cytokines whose expression is dependent on the activation of calcineurin, interleukin-4 (IL-4) played a critical role in ATP-mediated cell survival of FDC.P2 cells because neutralizing antibody against IL-4 effectively abrogated the antiapoptotic activity of ATP. Moreover, ATP treatment induced a significant amount of secreted IL-4 that was sufficient to maintain cell viability. Taken together, our present results demonstrate that extracellular ATP triggers autocrine production of IL-4 through calcium-dependent activation of calcineurin and secreted IL-4 substitutes IL-3 in protecting FDC.P2 cells from apoptosis even in the absence of IL-3.

Adenosine Triphosphate↗
PubMed2005

Cryopreservation of cultured periosteum: effect of different cryoprotectants and pre-incubation protocols on cell viability and osteogenic potential.

Evidence has accumulated that periosteal cells have a great potential to regenerate bone. We have demonstrated that cultured periosteum (CP) in membrane form is an effective device to regenerate alveolar bone. To increase the availability of CP in a clinical environment, an effective cryopreservation protocol for CP has been developed. In this study, three different cryoprotectants (Me(2)SO, glycerol, and ethylene glycol) were used. The effect on cell viability of pre-incubation temperature, pre-incubation time, and agitation during incubation was investigated. Samples were stored at -196 degrees C for 10 days. Cell viability was assessed by a colorimetric cell viability assay using a tetrazolium salt, and the assay results were confirmed by confocal laser scanning microscopy after staining with a combination of calcein AM and ethidium homodimer-1. The activity of the cells after thawing was assessed by alkaline phosphatase assay. To assess the osteogenic potential of cryopreserved CP, the CP was grafted to calvarial defects in athymic rats. The greatest cell viability was obtained in the group equilibrated at 37 degrees C for 30 min with Me(2)SO, under agitation, showing 63.3 +/- 10.5% recovery. After cryopreservation, the cell growth of surviving cells was identical when Me(2)SO was used as a cryoprotectant. Alkaline phosphatase (ALP) activity was maintained in the groups cryopreserved with Me(2)SO and glycerol. The transplantation experiment showed that the calvarial defects were completely closed by grafting cryopreserved CP, which demonstrates that the osteogenic property of CP was well maintained. An efficient cryopreservation protocol for CP has been developed and this will provide a convenient and effective treatment option for bone regeneration in clinics.

Alkaline Phosphatase↗
PubMed2003

Divergence in signaling pathways involved in promotion of cell viability mediated by bFGF, NGF, and EGF in PC12 cells.

We employed a series of inhibitors of intracellular cascade to disclose the precise molecular mechanisms by which basic fibroblast growth factor (bFGF) promotes viability of PC12 cells and compared with nerve growth factor (NGF) and epidermal growth factor (EGF). The MEK 1 and 2 inhibitors, U0126 and PD98059, significantly suppressed cell viability mediated by bFGF in a dose-dependent manner, and to a greater extent compared with EGF and NGF. The degree of MEK dependency for growth factor-mediated cell viability was estimated to be in the order of bFGF, EGF, and NGF. Rapamycin strongly inhibited the effect of NGF on cell viability, compared with bFGF and EGF. The mechanisms of action of NGF-mediated cell viability may depend largely on p70 S6 kinase-related signal transduction pathways comparing to bFGF and EGF. The present findings suggest that different signal transduction systems may be involved in the molecular mechanisms by which bFGF, NGF, and EGF mediate cell viability.

Animals↗
PubMed1978

Cell viability studies on the exfoliated colonic cancer cell.

Suspensions of desquamated colonic cancer cells were obtained from patients with cancer of the large bowel by colonic exfoliative cytology and from resected specimens of colonic cancer by an exfoliative technique. In addition, a tumor suspension was obtained from the resected specimens. Cell viability studies were performed on these cell suspensions. Whereas 23 of the 25 tumour homogenate cell suspensions were shown to exclude trypan blue, none of the exfoliated colonic cancer cell suspensions had viable cells. This finding would cast some doubt on the hypothesis that suture line recurrence following large bowel cancer surgery is due to the implantation of cells desquamated from the surface of the growth.

Cell Separation↗
PubMed1997

Effects of eosinophil granule proteins on human corneal epithelial cell viability and morphology.

PURPOSE: There is mounting evidence that eosinophil granule proteins may cause tissue injury during allergic inflammation of the eye. Therefore, the authors investigated the in vitro effects of human eosinophil major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO), and eosinophil-derived neurotoxin (EDN) on cultured human corneal epithelial cell viability and morphology. METHODS: Confluent primary human corneal epithelial cell cultures were exposed to each of the four human eosinophil cationic granule proteins at concentrations ranging from 0 to 100 micrograms/ml (0, 12.5, 25, 50, and 100 micrograms/ml) for up to 48 hours in serum-free media. Morphologic changes were assessed by light microscopy at 1, 6, 24, and 48 hours; cell viability was measured using the MTT cell viability assay at 24 hours. RESULTS: Cells treated with MBP and ECP induced a dose-dependent gradual increase in morphologic changes; in contrast, EPO and EDN induced minimal changes in cell morphology. At 24 hours, both MBP and ECP induced statistically significant (P < 0.05) decreases in cell viability at a concentration of 100 micrograms/ml; EPO induced a significant (P < 0.05) decrease in cell viability at all concentrations tested, and EDN showed no significant reduction of cell viability at any of the concentrations tested. CONCLUSIONS: The current study suggests that the human eosinophil granule proteins MBP and ECP affect human corneal epithelial cell viability and morphology in vitro, whereas the protein EPO affects cell viability only. EDN had no significant effect on cell viability or morphology. Hence, MBP, ECP, and EPO perturb the corneal epithelium differentially and may contribute to keratopathy associated with severe ocular allergy.

Blood Proteins↗
PubMed1999

Involvement of ppGpp, ribosome modulation factor, and stationary phase-specific sigma factor sigma(S) in the decrease in cell viability caused by spermidine.

Accumulation of spermidine in Escherichia coli causes a decrease in cell viability at the late stationary phase of cell growth. The mechanism underlying this effect has been studied. Spermidine accumulation caused an increase in the level of ppGpp and a decrease in ribosome modulation factor (RMF) and stationary phase-specific sigma factor sigma(S), both of which are believed to be involved in cell viability. Transformation of E. coli with the gene for stringent factor, which synthesizes ppGpp, also caused a significant decrease in the levels of RMF and sigma(S) factor and a decrease in cell viability. The results strongly suggest that the accumulation of ppGpp is also involved in the decrease in cell viability and that the sigma(S) factor assists the function of RMF in cell viability.

Bacterial Proteins↗
PubMed1984

A comparative study of the effects of mercury compounds on cell viability and nucleic acid synthesis in HeLa cells.

The effects of various mercury compounds on HeLa cell viability and DNA and RNA syntheses in intact cells and in isolated nuclei have been studied. The compounds examined were: methylmercuric chloride, ethylmercuric chloride, dimethylmercury, phenylmercuric acetate, p-hydroxymercuribenzoate, p-hydroxymercuribenzenesulfonate, HgCl2, HgSO4 , Hg(ClO4)2 and Hg2(ClO4)2. All of the compounds except dimethylmercury inhibited colony formation as well as DNA synthesis in intact cells and in isolated nuclei. RNA synthesis in intact cells was inhibited by all the compounds except dimethylmercury, p-hydroxymercuribenzoate and Hg(ClO4)2. In isolated nuclei, alpha-amanitin-resistant RNA synthesis was inhibited by all the compounds except dimethylmercury, alpha-Amanitin-sensitive RNA synthesis was stimulated by some compounds, inhibited by some, and unaffected by others. The effects of two non-mercurial sulfhydryl reagents, N-ethylmaleimide and iodoacetic acid, were also examined. These compounds showed a pattern of effects on nucleic acid synthesis which differed considerably from that of the mercury compounds. Neither compound significantly inhibited alpha-amanitin-resistant RNA synthesis in isolated nuclei, although both inhibited RNA synthesis in intact cells. Iodoacetic acid had no inhibitory effect on DNA synthesis in isolated nuclei but strongly inhibited DNA synthesis in intact cells.

Cell Survival↗
PubMed1978

Biochemical studies on liver functions in primary cultured hepatocytes of adult rats. I. Hormonal effects on cell viability and protein synthesis.

Liver parenchymal cells were isolated from adult rats by digesting liver slices or perfusing liver with collagenase. The cell yields were 1.5 X 10(7) and 1.0 X 10(8) cells/g liver from slices and perfused liver, respectively, and in both cases the cell viabilities and attachment efficiencies were over 90% and 60%, respectively. The cells were viable for more than one week when cultured in Williams medium E with 10% fetal bovine serum, and addition of insulin and dexamethasone enhanced the maintenance of cell viability. Various biochemical functions or freshly isolated cells and cultured cells were compared in this medium. In freshly isolated cells, induction of tyrosine transaminase [EC 2.6.1.5] by dexamethasone was low and none of the hormones examined stimulated protein synthesis; but when the cells had been cultured for a few days, induction of tyrosine transaminase became prominent, and insulin and dexamethasone stimulated protein synthesis and glucagon inhibited their effect. About half the synthesized proteins were secreted into the medium and among these proteins, albumin, transferrin, fibrinogen, and lipoproteins were identified immunochemically and electrophoretically. It was also shown that the polysomes in freshly isolated cells were almost completely disaggregated, but that in cells after a few days culture they were reaggregated. These results showed that freshly isolated cells have impaired functions, but that after culture for a few days the cells recover various liver functions and thus become more suitable for use in biochemical studies on liver functions.

Animals↗
PubMed2006

IL-1beta-induced iNOS expression, NO release and loss in metabolic cell viability are resistant to inhibitors of ceramide synthase and sphingomyelinase in INS 832/13 cells.

CONTEXT: Emerging evidence indicates regulatory roles for ceramide in the metabolic dysfunction of the islet beta cell. Recently, potential similarities between IL-1beta and ceramide on their effects on islet beta cell have been reported, including reduction in mitochondrial membrane potential and loss in metabolic cell viability. OBJECTIVE: Herein, we investigated whether IL-1beta-induced nitric oxide synthetase (iNOS) expression, nitric oxide (NO) release and loss in metabolic cell viability require ceramide biosynthesis either via the activation of sphingomyelinase or ceramide synthase. SETTING: Insulin-secreting INS 832/13 cells. RESULTS: We found that two structurally-distinct inhibitors of sphingomyelinase activation (e.g., 3-O-methylsphingomyelin or desipramine) or ceramide biosynthesis inhibitor (e.g., fumonisin) failed to exert clear effects on IL-1beta-induced iNOS expression, NO release and loss in cell viability. CONCLUSIONS: Taken together, our findings indicate that neither the sphingomyelinase nor the ceramide synthase activation is required for IL-1beta-induced metabolic abnormalities in insulin-secreting INS 832/13 cells.

Animals↗
PubMed2001

Quiescence, cell viability, apoptosis and necrosis of smooth muscle cells using different growth inhibitors.

Smooth muscle cells and endothelial cells play an important role in cardiovascular diseases and may therefore be a potential target for gene therapy. Most in vitro experiments are performed using proliferating cell cultures. Nevertheless, non-dividing cells would represent more realistic in vivo conditions for gene therapy. Therefore, a simple method to achieve physiologically quiescence in cell cultures is needed for experiments. Growth to confluence is sufficient for endothelial cells to reach quiescence, in contrast to smooth muscle cells. Alternative techniques were investigated to achieve quiescence for smooth muscle cells. N-acetyl-cysteine, heparin, aphidicolin and serum-free medium are known inhibitors of smooth muscle cell proliferation and were tested for cell viability, necrosis and apoptosis. The inhibition status was evaluated counting cells in a cell counter. Toxicity, necrosis and apoptosis were determined using FACS analysis. Then, smooth muscle cells and endothelial cells were transfected with plasmid containing the beta-galactosidase gene using liposomes. Analysis of gene expression in transfected cells included a quantitative beta-galactosidase assay and X-gal staining. Growth inhibition was achieved with all agents tested. Using N-acetyl-cysteine, only slightly reduced growth rates were observed. Aphidicolin stopped cell growth almost immediately, but demonstrated enhanced toxicity. The amount of apoptotic and necrotic cells was lowest using heparin in the presence of foetal calf serum. Transfection experiments using stationary cultures of smooth muscle cells using heparin or aphidicolin demonstrated 5-10-fold lower transfection rates compared to transfected proliferating cell cultures serving as controls. Transfection experiments using stationary cultures of endothelial cells using growth inhibition through confluence demonstrated 40-fold lower transfection rates than transfected proliferating cell cultures. Transfer efficiency was much lower in endothelial cells compared to smooth muscle cells. In conclusion, quiescent cells simulate more realistically the in vivo situation and may therefore represent a better model for future in vivo experiments based on in vitro findings.

Animals↗
PubMed2006

Rat spinal motion segment in organ culture: a cell viability study.

STUDY DESIGN: This study investigated tissue integrity and viability of cells in an organ culture system of intervertebral disc (IVD) with adjoining vertebral bodies. OBJECTIVE: The goal of this study was to design a methodology to maintain an IVD motion segment in organ culture, thereby preserving viability and tissue architecture. SUMMARY OF BACKGROUND DATA: Study of IVD mechanobiology in vitro necessitates availability of vertebral bodies for controlled application of complex loads. METHODS: IVD motion segments were dissected from rat lumbar segments and maintained in organ culture and cell viability was evaluated histochemically using NitroBlue Tetrazolium. Tissue integrity and morphology were evaluated using conventional histologic techniques. RESULTS: The in vitro organ culture of motion segments maintained the viability and tissue integrity for 14 days. More than 95% viability in all three regions of interest (anulus fibrosus, nucleus pulposus, end plates) was maintained for 14 days in culture. CONCLUSION: Our initial results suggest that long-term motion segment culture is practical, and the inclusion of vertebral bodies will facilitate anchoring during biomechanical stimulation. Thus, we expect the culture system to provide us with an excellent model for studying the pathomechanics of IVD degeneration and the effects of mechanical stimulation on the biology of IVD cells.

Animals↗
PubMed2006

Differential involvement of intracellular Ca2+ in 1-methyl-4-phenylpyridinium- or 6-hydroxydopamine-induced cell viability loss in PC12 cells.

1-Methyl-4-phenylpyridinium (MPP(+)) or 6-hydroxydopamine (6-OHDA) caused a nuclear damage, the mitochondrial membrane permeability changes, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species and the depletion of GSH in PC12 cells. Nicardipine (a calcium channel blocker), EGTA (an extracellular calcium chelator), BAPTA-AM (a cell permeable calcium chelator) and calmodulin antagonists (W-7 and calmidazolium) attenuated the MPP(+)-induced mitochondrial damage and cell death. In contrast, the compounds did not reduce the toxicity of 6-OHDA. Treatment with MPP(+ )or 6-OHDA evoked the elevation of intracellular Ca(2+) levels. Unlike cell injury, addition of nicardipine, BAPTA-AM and calmodulin antagonists prevented the elevation of intracellular Ca(2+) levels due to both toxins. The results show that the MPP(+)-induced formation of the mitochondrial permeability transition seems to be mediated by elevation of intracellular Ca(2+) levels and calmodulin action. In contrast, the 6-OHDA-induced cell death seems to be mediated by Ca(2+)-independent manner.

1-Methyl-4-phenylpyridinium↗
PubMedDate not supplied

Radiolabeled red cell viability. II. 99mTc and 111In for measuring the viability of heterologous red cells in vivo.

The authors developed a double in vivo crossmatch method using 2 to 3 ml of potential donor blood labeled with either 400 microCi of 99mTc or 30 microCi of 111In-oxine. Data are presented for 19 crossmatches on nine patients, using one blood specimen labeled with 99mTc or two specimens, one labeled with 99mTc and the other with 111In. Normal values are given for standardization purposes. This method appears to have advantages over earlier in vivo crossmatch techniques using 51Cr-labeled RBCs. These advantages include the rapidity with which the in vivo crossmatch may be repeated, the ready availability of 99mTc and 111In-oxine, and the lower radiation absorbed doses with the shorter-lived radionuclides.

Cell Survival↗
PubMed2006

Stat3 activation is required for cell proliferation and tumorigenesis but not for cell viability in cutaneous squamous cell carcinoma cell lines.

Signal transducer and activator of transcription 3 (Stat3), a cytoplasmic transcription factor, is constitutively activated in various types of cancer. Previous investigations have demonstrated that Stat3 plays important roles in cell growth, survival, differentiation, and transformation. The constitutive activation of Stat3 in human malignancies is an important key to maintain the characteristics of a malignant tumor, such as the rate of proliferation and/or immortalization, and inhibition of Stat3 function could be a potent therapeutic approach. In order to elucidate the role of Stat3 in tumors, cutaneous squamous cell carcinoma (SCC) cells, which have constitutive activation of Stat3 in vivo and in vitro, were used for this study. To investigate the effect of specific inhibition of Stat3 in SCC cells, we developed small interfering RNAs (siRNAs) that target Stat3, and which effectively prevent its expression in vitro. Introduction of Stat3 siRNA into SCC cells led to inhibition of growth and changes in morphology but did not induce apoptosis. Stat3 siRNA-transfected SCC cells had impaired tumor growth in nude mice. These findings demonstrate that Stat3 plays a critical role in the tumorigenesis, but not in the cell survival, of SCC cells and suggest that additional pro-apoptotic signals are necessary for the induction of apoptosis.

Animals↗
PubMed1990

Extracellular calcium effects on cell viability and thiol homeostasis.

Studies of chemically induced cell injury and death, which have used as model systems freshly isolated rat hepatocytes and hepatocytes in culture, are discussed. An important model uses the omission of Ca2+ from the medium during rat hepatocyte incubations. Ca2+ omission induces an intense oxidative stress within hepatocytes incubated in a 95% O2 + 5% CO2 atmosphere. The relationship of calcium homeostasis to the parameters of oxidative stress is important to understanding the progression from reversible to irreversible injury. In the Ca2+ omission model, the vitamin E (Vit. E) content of hepatocytes is important for the prevention of cell injury. Recent studies with rat hepatocytes show that ruthenium red (RR) and La3+, which block Ca2+ translocation through the mitochondrial uniport, can prevent malondialdehyde (MDA) formation, reduced glutathione (GSH), and protein-SH loss, Vit. E loss, and LDH leakage induced by Ca2+ omission from the incubation medium. Ca2+ omission promoted a marked loss of mitochondrial transmembrane potential (delta phi) that was prevented by RR, EGTA, Vit. E, and desferrioxamine. The absence of extracellular Ca2+ may cause mitochondrial Ca2+ cycling that contributes to the observed oxidative stress, resultant loss of cell viability, and protein thiol homeostasis. Chemical agents including a glutathione-depleting agent, ethacrynic acid, and a redox cycling agent, adriamycin, increase the loss of cell viability caused by a Ca2(+)-free medium, but they have some additional effects on cellular processes. The demise of cell viability by the agent is also preventable by Vit. E supplementation. Ca2+ has a role in cell injury that appears to uniquely involve mitochondrial homeostasis.

Animals↗