W1703 Survivin is a Key Factor in the Differential Susceptibility of Gastric Endothelial and Epithelial Cells to Alcohol-Induced Injury

Jones, Michael K.; Padilla, Oscar R.

doi:10.1016/s0016-5085(10)63323-9

Cited by 5 publications

(6 citation statements)

References 23 publications

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“…A protective effect of survivin on ethanol susceptibility at ethanol concentrations of 1%–5% was found by Jones et al in gastric endothelial and epithelial cells of the rat 13,14. We found a statistically significant decrease in survivin expression after resveratrol treatment compared to the ethanol control.…”

Section: Discussionsupporting

confidence: 76%

Resveratrol decreases B-cell lymphoma-2 expression and viability in GH3 pituitary adenoma cells of the rat

Voellger¹,

Kirches²,

Wilisch‐Neumann³

et al. 2013

OTT

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ObjectiveResveratrol is a phytoestrogen with various antiproliferative and proapoptotic effects. This in vitro study aimed to analyze the effect of resveratrol on the viability and expression of modulators of apoptosis in GH3 pituitary adenoma cells of the rat.MethodsGH3 cells were incubated with resveratrol concentrations from 20 to 100 μM for 48–72 hours. Cell viability was quantified using a hemocytometer. We assessed the ability of resveratrol to kill GH3 cells by an enzyme-linked immunosorbent assay (ELISA) of nucleosome liberation and by DNA degradation (unidimensional gel electrophoresis). Relative messenger RNA (mRNA) expression of survivin, B-cell lymphoma-2 protein (BCL-2) and BCL-2-associated X protein (BAX) normalized to β2 microglobulin was measured using quantitative real-time polymerase chain reaction (qRT-PCR).ResultsGH3 cell survival significantly decreased with increasing concentrations of resveratrol. In GH3 cells treated with 100 μM resveratrol, ELISA demonstrated a significant rise of nucleosome liberation, which typically occurs during apoptosis. In parallel, gel electrophoresis showed degradation of DNA into random fragments, pointing to a necrotic mode of cell death in most GH3 cells. In GH3 cells treated with 100 μM resveratrol, qRT-PCR detected a significant decrease of BCL-2 mRNA expression and a decrease of survivin mRNA expression, whereas a change of BAX mRNA expression could not be found. The BAX/BCL-2 ratio was significantly increased in GH3 cells after resveratrol treatment.ConclusionsResveratrol reduces GH3 cell viability in a dose-dependent manner by inducing nonapoptotic cell death and apoptosis. Apoptosis in GH3 cells is probably mediated by resveratrol-dependent downregulation of apoptosis inhibitors, namely BCL-2 and possibly survivin. Further investigation of the potential effects of resveratrol on pituitary adenoma cells is warranted.

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Section: Discussionsupporting

confidence: 76%

Resveratrol decreases B-cell lymphoma-2 expression and viability in GH3 pituitary adenoma cells of the rat

Voellger¹,

Kirches²,

Wilisch‐Neumann³

et al. 2013

OTT

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“…Moreover, survivin expression in endothelial cells was reportedly much lower than that in epithelial cells under physiological conditions. 24 Thus, bronchial epithelial cells may be the main source of survivin mRNA seen in control lung samples (Figure 3e), results that (Figures 1a and b). As lung epithelial cells, especially bronchial epithelial cells in small airways, have an important function in defending the lung parenchyma against apoptotic stimuli such as physical oxidants, dusts, and infectious insults, it is tempting to speculate that cytoplasmic survivin in bronchial epithelial cells contributes to a constitutive antiapoptotic activity that would benefit the integrity and physiological functioning of the lung.…”

Section: Discussionmentioning

confidence: 74%

Role of survivin in acute lung injury: epithelial cells of mice and humans

Terasaki

Urushiyama

et al. 2013

Laboratory Investigation

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Survivin, an inhibitor of apoptosis, regulates cell division and is a potential target for anticancer drugs because many cancers express high survivin levels. However, whether survivin would be toxic to human lung cells and tissues has not been determined. This report clarified the involvement of survivin in acute lung injury. We used immunohistochemical analysis, immunoelectron microscopy, and real-time reverse transcription-quantitative polymerase chain reaction to study survivin expression and localization in injured mouse and human lungs. We also used cultured human lung epithelial cells (BEAS-2B and A549) to study survivin cytoprotection. Nuclei and cytoplasm of epithelial cells in day 3 and day 7 models of bleomycin-injured lung showed survivin-positive results, which is consistent with upregulated survivin mRNA expression. These nuclei also evidenced double positive findings for proliferating cell nuclear antigen and survivin. Day 7 models had similar Smac/DIABLO-positive and survivin-positive cell distributions. The cytoplasm and nuclei of epithelial cells in lesions with diffuse alveolar damage manifested strong survivin-positive findings. Bleomycin stimulation in both epithelial cell lines upregulated expression of survivin and apoptosis-related molecules. Suppression of survivin expression with small interfering RNA rendered human lung epithelial cells susceptible to bleomycin-induced damage, with markedly upregulated activation of caspase-3, caspase-7, poly (ADP-ribose) polymerase, and lactate dehydrogenase activity and an increased number of dead cells compared with mock small interfering RNA-treated cells. Overexpression of survivin via transfection resulted in these epithelial cells being resistant to bleomycin-induced cell damage, with reduced activation of apoptosis-related molecules and lactate dehydrogenase activity and fewer dead cells compared with results for mock-transfected cells. Survivin, acting at the epithelial cell level that depends partly on apoptosis inhibition, is therefore a key mediator of cytoprotection in acute lung injury. Understanding the precise role of survivin in normal lung cells is required for the development of therapeutic survivin.

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“…Wee1 has been reported to inhibit CDK1 activity by phosphorylation (Chow and Poon, 2012;Magnussen et al, 2012), which in turn decreases survivin (Chen et al, 2013) and consequently activates Caspase-3 (Jones et al, 2010;Rubio et al, 2012). The phosphorylation of CDK1 and decrease in survivin are also involved in the mechanism of apoptosis via mitotic catastrophe (Castedo et al, 2004;Lamers et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Wee1 in the Circadian Rhythm–Dependent Intestinal Damage Induced by Docetaxel

Obi-Ioka¹,

Ushijima²,

Kusama³

et al. 2013

J Pharmacol Exp Ther

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Docetaxel, a semisynthetic taxane, is effective for the treatment of some solid cancers; however, docetaxel-induced intestinal damage leads to poor prognosis in some patients. Although such adverse effects have been reported to depend on the dosing-time of docetaxel, the mechanisms involved remain unclear. Wee1 expression is controlled by the clock gene complex, clock/bmal1, and contributes to cell-cycle progression. The present study was undertaken to evaluate the potential role of Wee1 in the circadian rhythm-dependent profile of docetaxel. Male mice were maintained under a 12-hour light/ dark cycle. Intestinal damage after repeated dosing of docetaxel (20 mg/kg) for 3 weeks was more severe at 14 hours after light on (HALO) than at 2 HALO. The intestinal protein expressions of Wee1, phosphorylated CDK1, and cleaved Caspase-3 were higher in the 14-HALO group than in the 2-HALO group, whereas that of survivin was lower in the 14-HALO group. Thus, it is speculated that elevated Wee1 expression inhibited CDK1 activity more by phosphorylation, which in turn caused the lower expression of survivin and consequently more activated Caspase-3 in the 14-HALO group. There were no significant differences in plasma docetaxel concentrations between the 2-and 14-HALO groups. Bindings of CLOCK and BMAL1 to the E-box regions at the wee1 gene promoter were not altered by docetaxel treatment at 2 and 14 HALO. These findings suggest that Wee1 is directly or indirectly involved in the mechanism of the circadian rhythm-dependent changes in docetaxel-induced intestinal damage. However, the mechanism for a circadian rhythm-dependent change in intestinal Wee1 expression by docetaxel remains to be determined.

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W1703 Survivin is a Key Factor in the Differential Susceptibility of Gastric Endothelial and Epithelial Cells to Alcohol-Induced Injury

Cited by 5 publications

References 23 publications

Resveratrol decreases B-cell lymphoma-2 expression and viability in GH3 pituitary adenoma cells of the rat

Resveratrol decreases B-cell lymphoma-2 expression and viability in GH3 pituitary adenoma cells of the rat

Role of survivin in acute lung injury: epithelial cells of mice and humans

Involvement of Wee1 in the Circadian Rhythm–Dependent Intestinal Damage Induced by Docetaxel

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