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Journal of Environmental Pathology, Toxicology and Oncology

Published 4 issues per year

ISSN Print: 0731-8898

ISSN Online: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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The Role of Nitric Oxide and Cyclooxygenase-2 in Attenuating Apoptosis

Volume 21, Issue 2, 2002, 10 pages
DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i2.30
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ABSTRACT

The production of nitric oxide (NO) is an essential determinant in auto- and paracrine signaling. NO is generated under inflammatory conditions and may serve as a cytotoxic molecule to produce cell demise along an apoptotic or necrotic pathway. NO also gained attention as a regulator of immune function and a death inhibitor. Cytotoxicity because of substantial NO-formation is established to initiate apoptosis, characterized by upregulation of the tumor suppressor p53, changes in the expression of pro- and antiapoptotic Bcl-2 family members, cytochrome с relocation, activation of caspases, and DNA fragmentation. However, NO-toxicity is not a constant value and NO may protect several cell types from entering programmed cell death. Preactivation of macrophages with a nontoxic dose of S-nitrosoglutathione (200 mM) or lipopolysaccharide/interferon-g/NG-monomethyl-L-arginine for 15 hours attenuated death in response to various agonists, suppressed p53 accumulation, and abrogated caspase activation. Prestimulation of macrophages with cytokines or low-level NO activated the transcription factor NF-kВ as well as AP-1 and promoted immediate early gene expression of cyclooxygenase-2 (COX-2). NF-kВ activation comprised p50/p65-heterodimer formation, IkВ degradation, and activation of a luciferase reporter construct, that contained four copies of the NF-kВ-site derived from the murine COX-2 promoter. A NF-kВ decoy approach (oligonucleotides directed against NF-kВ) or transfection of a dominant-negative c-Jun mutant (TAM67) abrogated not only the COX-2 expression but also the inducible protection. Blocking NO- or cytokine-mediated inducible protection at the level of NF-kВ and/or AP-1 restored the occurrence of apoptotic features. Our experiments underscore the role of COX-2 in attenuating natural occurring cell death (i.e., apoptosis).

CITED BY
  1. Johnson Lori, Gibson Angelia, Maung Kavita, O'Shaughnessy Joyce, 2002 Highlights from: 38th Annual Meeting of the American Society of Clinical Oncology, Orlando, Florida, May 18–21, 2002, Clinical Breast Cancer, 3, 3, 2002. Crossref

  2. Johnson Lori, Maung Kavita, Chu Edward, Highlights From: 38th Annual Meeting of the American Society of Clinical Oncology; Orlando, Florida May 18–21, 2002, Clinical Colorectal Cancer, 2, 2, 2002. Crossref

  3. Vignola A. M., Bellia V., Transcriptional regulation of COX-2: a key mechanism in the pathogenesis of nasal polyposis in aspirin-sensitive asthmatics?, Allergy, 58, 2, 2003. Crossref

  4. Ríos José Luis, Recio M. Carmen, , 33, 2006. Crossref

  5. NORDBORG C., AMAN P., PERSSON M., NORDBORG E., Cell-type-specific expression of p53 and p21 in giant cell arteritis, APMIS, 113, 9, 2005. Crossref

  6. Karpuzoglu Ebru, Ahmed S. Ansar, Estrogen regulation of nitric oxide and inducible nitric oxide synthase (iNOS) in immune cells: Implications for immunity, autoimmune diseases, and apoptosis, Nitric Oxide, 15, 3, 2006. Crossref

  7. Gangoiti Patricia, Granado Maria H., Arana Lide, Ouro Alberto, Gómez-Muñoz Antonio, Involvement of nitric oxide in the promotion of cell survival by ceramide 1-phosphate, FEBS Letters, 582, 15, 2008. Crossref

  8. Cristina Cerquetti M., Hovsepian Eugenia, Sarnacki Sebastian H., Goren Nora B., Salmonella enterica serovar Enteritidis dam mutant induces low NOS-2 and COX-2 expression in macrophages via attenuation of MAPK and NF-κB pathways, Microbes and Infection, 10, 14-15, 2008. Crossref

  9. Hu Maowen, Miller Edmund J, Lin Xinchun, Simms H.Hank, Transmigration across a lung epithelial monolayer delays apoptosis of polymorphonuclear leukocytes, Surgery, 135, 1, 2004. Crossref

  10. Wang X, Zalcenstein A, Oren M, Nitric oxide promotes p53 nuclear retention and sensitizes neuroblastoma cells to apoptosis by ionizing radiation, Cell Death & Differentiation, 10, 4, 2003. Crossref

  11. Du Yunpeng, Sarthy V. P., Kern T. S., Interaction between NO and COX pathways in retinal cells exposed to elevated glucose and retina of diabetic rats, American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 287, 4, 2004. Crossref

  12. Dazard Jean-Eudes, Gal Hilah, Amariglio Ninette, Rechavi Gideon, Domany Eytan, Givol David, Genome-wide comparison of human keratinocyte and squamous cell carcinoma responses to UVB irradiation: implications for skin and epithelial cancer, Oncogene, 22, 19, 2003. Crossref

  13. Hortelano Sonsoles, Través Paqui G., Zeini Miriam, Alvarez Alberto M., Boscá Lisardo, Sustained Nitric Oxide Delivery Delays Nitric Oxide-Dependent Apoptosis in Macrophages: Contribution to the Physiological Function of Activated Macrophages , The Journal of Immunology, 171, 11, 2003. Crossref

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