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1.
Journal of International Oncology ; (12): 483-485, 2008.
Artigo em Chinês | WPRIM | ID: wpr-399535

RESUMO

Oncolytic adenovirus-mediated E1A gene therapy may be a useful therapeutic approach for cancer treatment.In addition to direct lysis,viruses also mediate exogenous tumor suppressor genes inducing antitumor efficacy.Vectors need further investigation to improve the targeting and effectiveness in vivo.

2.
Chinese Journal of Microbiology and Immunology ; (12): 416-420, 2008.
Artigo em Chinês | WPRIM | ID: wpr-382142

RESUMO

Objective To analyze the influence of adenovirus latent infection on gamma-glutamylcysteine systhetase(γ-GCS) in rat alveolar epithelial cells. Methods The rat alveolar epithelial cells were stably transfected with the plasmid pE1Aneo and control plasmid. Glutathione(GSH) contents, the activity of γ-GCS were detected in oxidant stress. Then the leuel of protein expression, mRNA expression, and promoter transcriptional activity of glutamate-cysteine ligase catalytic subunit(GCLC) were further detected. Results GSH contents decreased because of adenovirus E1A expression in oxidant stress. E1A repressed the expression and activity of γ-GCS, messenger RNA expression, and promoter transcriptional activity of GCLC. Conclusion Adenovirus E1A decreased the activity of γ-GCS probably by repressed promoter transcriptional activity of GCLC. As a result, GSH contents were downregulated in oxidant stress. Thus Adenovirus latent infection amplified the oxidant/antioxidant imbalance in rat alveolar epithelial cells in oxidants stress, which may be an important mechanism of COPD.

3.
Chinese Journal of Immunology ; (12)2001.
Artigo em Chinês | WPRIM | ID: wpr-545576

RESUMO

Objective:To explore the expression of intercellular adhesion molecule-1(ICAM-1 )induced by cigarette smoking extract(CSE) as well as the influence of the adenovirus E1A gene in pulmonary epithelial cells.Methods:A549 cells were transfected with a plasmid carrying the adenovirus E1A gene and stable trasfectants expressing E1A protein were selected. The cells were tested for the expression of ICAM-1 after stimulation with different concentrations of CSE.Results:ICAM-1expression was increased in A549 markedly with CSE stimulation,and the higher CSE concentration were,the more expression of ICMA-1 was observed. As compared with parental cells or cells transfected with control plasmid, ICAM-1 expression was markedly increased with stimulation of different concentrations of CSE in E1A-positive A549 cells.Conclusion:CSE exposure induces the surface expression of ICAM-1 and adenovirus E1A gene can markedly increase ICAM-1 expression induced by CSE in pulmonary epithelial cells, which suggest that latent adenovirus infection may amplify the inflammation process present in airways of smokers.

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