Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08758 (annexin V)
 9,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isatin is an endogenous indole that is increased in stress, inhibits monoamine oxidase (MAO) B and improves bradykinesia and striatal dopamine levels in rat models of Parkinson's disease. Consequently, it has been suggested that isatin might be a possible treatment for Parkinson's disease although little is known about its effects on neural cell growth and survival. The aim of this study was to investigate the survival of dopaminergic human neuroblastoma (SH-SY5Y) cells following treatment with increasing concentrations of isatin. SH-SY5Y cells were exposed to isatin for defined time points, after which cell survival was determined by MTT assay. A combination of Annexin V binding and propidium iodide (PI) exclusion was used to distinguish apoptosis from necrosis in flow cytometry experiments and FACS profiles of permeabilised PI-labelled cells were employed for the assessment of cell cycle distribution. Isatin treatment (1-400 microM) for 24h induced a significant dose-dependent increase in MTT metabolism by SH-SY5Y cells in culture, but this was not due to an increase in cell division. At the higher concentrations (200-400 microm) isatin triggered cell death, although MTT metabolism was still increased in the culture, suggesting that surviving cells were hypermetabolic. Following a longer (48 h) exposure, isatin was found to cause cell death in a dose-dependent manner; at lower concentrations (50 microM), the predominant mode of cell death was apoptosis while at the highest concentration (400 microm) increasing numbers of necrotic cells were also evident. Thus, in dopaminergic SH-SY5Y cells isatin induces cell death in dose- and time-dependent manner. This death occurred as a continuum of survival, apoptosis and necrosis. Our results re-emphasise that caution should be exercised when considering high doses of isatin as a putative anti-Parkinson's disease therapeutic.
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PMID:Isatin, an endogenous monoamine oxidase inhibitor, triggers a dose- and time-dependent switch from apoptosis to necrosis in human neuroblastoma cells. 1587 76

Ethanol induces oxidative stress in cultured fetal rat cortical neurons and this is followed by apoptotic death, which can be prevented by normalization of cell content of reduced glutathione (GSH). Because astrocytes can play a central role in maintenance of neuron GSH homeostasis, the following experiments utilized cocultures of neonatal rat cortical astrocytes and fetal cortical neurons to determine if astrocytes could protect neurons from ethanol-mediated apoptotic death via this mechanism. In cortical neurons cultured in the absence of astrocytes, ethanol (2.5 and 4 mg/ml; 6-, 12-, and 24-hr exposures) decreased trypan blue exclusion and the MTT viability measures by up to 45% (P < 0.05), increased levels of reactive oxygen species (ROS) by up to 81% (P < 0.05), and decreased GSH within 1 hr of treatment by 49 and 51% for 2.5 and 4 mg/ml, respectively (P < 0.05). This was followed by onset of apoptotic cell death as determined by increased Annexin V binding and DNA fragmentation by 12 hr of ethanol exposure. Coculturing neurons with astrocytes prevented GSH depletion by 2.5 mg/ml ethanol, whereas GSH content was increased over controls in neurons exposed to 4 mg/ml ethanol (by up to 341%; P < 0.05). Ethanol generated increases in neuron ROS and apoptosis; decreases in viability were also prevented by coculture. Astrocytes were largely insensitive to ethanol, using the same measures. Only exposure to 4.0 mg/ml ethanol decreased GSH content in astrocytes, concomitant with a 204% increase in GSH efflux (P < 0.05). These studies illustrate that astrocytes can protect neurons from ethanol-mediated apoptotic death and that this may be related to maintenance of neuron GSH.
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PMID:Astrocytes protect neurons from ethanol-induced oxidative stress and apoptotic death. 1588 May 62

A decoction of Nigella sativa seeds, Hemidesmus indicus root and Smilax glabra rhizome is used by traditional medical practitioners in Sri Lanka to treat cancer and has been shown to prevent chemically induced carcinogenesis in rats. The cytotoxicity of the decoction and the individual plant extracts were tested on the human hepatoma HepG2 cell line. The effects of 24 h incubation with different concentrations (0--50 mg/ml) of the extracts on HepG2 cells were determined. Results from MTT and SRB assays, and [(14)C]-leucine and [(3)H]-thymidine uptake demonstrated that the decoction had a strong dose-dependent cytotoxic activity. The greatest inhibitory effects were observed on DNA synthesis with both the decoction (91+/-S.E. 3.7% inhibition) and N. sativa plant extract (88+/-3.8%) even at low concentrations (5 mg/ml). The three individual plant extracts were cytotoxic in the order of potency N. sativa>H. indicus>S. glabra. Flow cytometric analysis using Annexin V and propidium iodide staining showed that after 24 h exposure to the decoction, cells were in the late stage of apoptosis and/or necrosis. Further experiments are worthwhile to determine the anticancer potential of this plant decoction and its components.
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PMID:Cytotoxic effects of a decoction of Nigella sativa, Hemidesmus indicus and Smilax glabra on human hepatoma HepG2 cells. 1591 74

PANcreatic DERived factor (PANDER, FAM3B) is a recently discovered islet-specific cytokine. We have previously shown that, in vitro, truncated recombinant PANDER isoforms (20 and 21 kDa) are cytotoxic to beta-cell lines but the effects of full-length PANDER on islet biology remain unclear. In this study, we used adenovirus (Ad-PANDER) to overexpress full-length cDNA of PANDER in islets and betaTC3 cells. BetaTC3 cells were infected with Ad-PANDER or control vector. After 48 h, cell viability was significantly decreased as evaluated by MTT assay. The number of dead cells was significantly increased as indicated by the fluorescent intensity of the propidium iodide-stained cells (160 +/- 13 vs. control 100 +/- 7%, P = 0.001). Flow cytometric Tunel assay showed that overexpressing PANDER induced a significant fourfold increase in beta-cell apoptosis (19.4 +/- 6.3 vs. control 4.1 +/- 0.8%, P < 0.05). There was a significant increase in the number of annexin V-positive (apoptotic) cells and propidium iodide-positive (dead) cells in mouse islets infected with Ad-PANDER compared with control cells infected with Ad-LacZ. Addition of 4 nM recombinant PANDER protein to betaTC3 cells or infection of Ad-PANDER did not affect Akt and STAT1 phosphorylation, Bcl-2, Fas, and NF-kappaB protein levels. However, activation of caspase-3 was observed in betaTC3 and islets infected with Ad-PANDER. Overexpression of PANDER in mouse islets or addition of recombinant PANDER decreased insulin secretion induced by carbachol plus glucose or high potassium but not that by glucose alone. Culture with recombinant PANDER did not affect glucose-induced NAD(P)H elevation in mouse islets. In conclusion, Ad-PANDER infection is as effective as truncated recombinant PANDER to induce betaTC3 cell and mouse islet apoptosis.
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PMID:Effects of overexpression of pancreatic derived factor (FAM3B) in isolated mouse islets and insulin-secreting betaTC3 cells. 1592 25

To investigate the apoptotic effect of triptolide on MDS cell line MUTZ-1 cells and its mechanism, MUTZ-1 cells were incubated with indicated concentrations of triptolide. The growth of MUTZ-1 cells was observed by MTT assay and apoptosis was detected by DNA fragmentation analysis and flow cytometry using Annexin V-FITC/PI staining. The gene and protein expressions were determined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot, respectively. The results showed that MUTZ-1 cell viability in presence of triptolide decreased markedly in a dose- and time-dependent manner. The growth-inhibitory IC50 value for triptolide treatment was 55.06 ng/ml. A DNA ladder pattern of internucleosomal fragmentation was observed. The translocation of phosphatidylserine at the outer surface of the cell plasma membrane could be induced by triptolide and its level increased following the augmentation of the drug concentration. Treatment of MUTZ-1 cells with triptolide for 12 hours resulted in the activation of caspase-3, cleavage of PARP and decrease of c-IAP2 mRNA. The expressions of pro-caspase 3 and c-IAP2 were inversely correlated with the incidence of apoptosis. (r = -0.907, P = 0.000; r = -0.919, P = 0.000 respectively). In conclusion, Triptolide inhibits MUTZ-1 cell growth by inducing apoptosis. The apoptotic effect of triptolide in MUTZ-1 cells is mediated by the caspase-3 activation and PARP cleavage. Moreover, the activation of caspase-3 may be associated with the down-regulation of c-IAP2.
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PMID:[Study of triptolide-induced apoptosis in MUTZ-1 cells and its allied mechanism]. 1597 36

Our previous study showed that arsenic trioxide (As2O3) was effective in inhibiting the growth of human hepatocellular carcinoma (HepG2) cells via induction of apoptosis. In the present study, we examined the effect of As2O3 on multidrug resistant human hepatocellular carcinoma (R-HepG2) cells which are characterized with overexpression of mdr1 gene and P-glycoprotein. The anti-proliferation of R-HepG2 by As2O3 was examined by MTT assay. For the induction of apoptosis, DNA fragmentation and Annexin V-PI staining were performed after treatment with arsenic trioxide. To study the effect of arsenic trioxide on P-glycoprotein, Western analysis probing anti-P-glycoprotein antibody was used to monitor the change of its expression. Results showed that As2O3 was effective in inhibiting the cell proliferation of R-HepG2 cells in a dose- and time-dependent manner via induction of apoptosis without affecting the cell cycle. The sensitivity of R-HepG2 cells toward As2O3 was found to be similar to that of the parental HepG2 cells. The Western analysis showed that As2O3 was probably not the substrate to be bound and extruded by P-glycoprotein in R-HepG2 cells because it could not maintain the cellular P-glycoprotein expression.
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PMID:Effect of arsenic trioxide on multidrug resistant hepatocellular carcinoma cells. 1598 6

The effects of insulin-like growth factor-1 (IGF-1) on the cytotoxicity and apoptosis induced by okadaic acid (OA) in SH-SY5Y cells were investigated. Cell viability was measured using the MTT (3-(4,5-dimethylthiazolyl-2)-2,-5-diphenyltetrazolium bromide) assay. Early and late apoptosis/necrosis were analyzed by flow cytometry using Annexin V and propidium iodide (PI) double-staining. Caspase-3 activation was detected by Western blot analysis. Preincubation with IGF-1 for 24 h prevented cytotoxicity induced by 40 nM OA given for 24 h, and the MTT value significantly increased. Incubation with 20 nM OA for 24 h caused a marked increase in the percentage of early apoptotic and late apoptotic/necrotic cells, which was not dependent on the activation of caspase-3. OA-induced apoptosis was significantly decreased by pretreatment with 10 ng/ml of IGF-1 for 24 h. The results supported the hypothesis that IGF-1 may be useful in the treatment of Alzheimer's disease.
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PMID:Effects of insulin-like growth factor-1 on okadaic acid-induced apoptosis in SH-SY5Y cells. 1608 62

Microparticles are small membrane vesicles released from the cell membrane by exogenous budding. To elucidate the interactions of microparticles with macrophages, the effect of microparticles released from Jurkat T cells on RAW 264.7 cells was determined. Microparticles were isolated by differential centrifugation, using FACS analysis with annexin V and cell surface markers for identification. Various inducers of apoptosis increased the release of microparticles from Jurkat cells up to 5-fold. The released microparticles were then cultured with RAW 264.7 cells. As shown by confocal microscopy and FACS analysis, RAW 264.7 macrophages cleared microparticles by phagocytosis. In addition, microparticles induced apoptosis in RAW 264.7 cells in a dose-dependent manner with up to a 5-fold increase of annexin V positive cells and 9-fold increase in caspase 3 activity. Cell proliferation as determined by the MTT test was also reduced. Furthermore, microparticles stimulated the release of microparticles from macrophages. These effects were specific for macrophages, since no apoptosis was observed in NIH 3T3 and L929 cells. These findings indicate that microparticles can induce macrophages to undergo apoptosis, in turn resulting in a further increase of microparticles. The release of microparticles from apoptotic cells may therefore represent a novel amplification loop of cell death.
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PMID:The release of microparticles by apoptotic cells and their effects on macrophages. 1613 65

Hematoporphyrin monomethyl ether (Hemoporfin) is a novel porphyrin-related photosensitizer. Photocytotoxic effect of Hemoporfin to ovarian cancer is still unclear. We used human epithelial ovarian carcinoma cell line SKOV3 and its xenograft model in nude mice to investigate the Hemoporfin-based photodynamic therapy (PDT) for ovarian cancer. The growth rates of SKOV3 cells were determined by MTT assays. Flow cytometry combined with dual Annexin V/PI staining was used to identify the death mode of the cells following PDT. We demonstrated that Hemoprofin-based PDT induced significant cell death via direct necrosis induction, and the photocytotoxity to SKOV3 cells is dose related. With SKOV3 xenograft model in nude mouse, we further demonstrated that Hemoporfin-based PDT is effective for controlling the tumor growth. Our results suggest that Hemoporfin is a promising novel photosensitizer for the treatment of ovarian cancer and merit further evaluation in the clinical practice.
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PMID:Phototoxicity of Hemoporfin to ovarian cancer. 1618 54

The purpose of this study was to investigate the cytotoxicity of iontophoresis treatment using direct current (DC) with or without antibacterial agents. The following antibacterial agents were used: diamine silver fluoride (AgF); sodium fluoride (NaF); and iodine zinc iodide (JJZ). The cytotoxic activity of DC with or without antibacterial agents against human polymorphonuclear cells (PMNs) was evaluated by the 3-[4, 5- dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay. It was noted that DC (2 mA) killed PMNs in a time-dependent manner and the cytotoxicity was enhanced when DC was combined with antibacterial agents. The toxic effect of antibacterial agents was in the order: AgF>JJZ>NaF. The death of PMNs by DC was evaluated by flow cytometry using annexin V-FITC/propidium iodide staining. DC appeared to induce necrosis rather than apoptosis of PMNs. These results suggest that iontophoresis treatment using DC and antibacterial agents may induce necrotic cytotoxicity in host cells around periapical lesions.
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PMID:Cytotoxicity of direct current with antibacterial agents against host cells in vitro. 1618 58


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