PGJ2 antagonizes NF-κB-induced HIV-1 LTR activation in colonic epithelial cells
Autor: | Stamatoula Pasvanis, Nancy Dumais, Sandra C. Côté, Benoit Barbeau, Salim Bounou, Amandine Vargas, Mélissa Boisvert |
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Rok vydání: | 2008 |
Předmět: |
Colon
Human immunodeficiency virus (HIV) Prostaglandin Biology medicine.disease_cause NF-κB Virus 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Transcription (biology) Virology medicine Humans Luciferases HIV Long Terminal Repeat PGJ2 030304 developmental biology Infectivity 0303 health sciences Luciferase reporter Prostaglandin D2 NF-kappa B HIV Epithelial Cells Molecular biology Mucosal transmission 3. Good health chemistry 030220 oncology & carcinogenesis HIV-1 lipids (amino acids peptides and proteins) Caco-2 Cells Transcription |
Zdroj: | Virology. 380(1):1-11 |
ISSN: | 0042-6822 |
DOI: | 10.1016/j.virol.2008.07.023 |
Popis: | Intestinal epithelial cells play an important role in early stages of HIV-1 infection and long-term persistence of the virus. Here we determined the mechanism that regulates HIV-1 activation via prostaglandin J(2) (PGJ(2)) in Caco-2 cells. We showed that treatment of Caco-2 cells with PGJ(2) decreased the infectivity of a luciferase reporter virus, pHXB-luc, as well as HIV production following infection of cells with a X4-tropic virus by antagonizing sodium butyrate, a cellular activator known to induce HIV-1 transcription. Transfection of intestinal epithelial cells such as Caco-2, HT-29 and SW620 cells with full-length HIV-1 LTR (pLTR-luc) revealed that PGJ(2) reduced HIV-1 LTR-mediated reporter gene activity. The involvement of NF-kappaB in the PGJ(2)-dependent down-regulation of HIV-1 transcription was further assessed using the kappaB-regulated luciferase-encoding vectors. In Caco-2 cells, PGJ(2) decreased IKK activity, resulting in reduced NF-kappaB translocation to the nucleus. Since sodium butyrate has been associated with a chronic stress response in AIDS patients, our results suggest that addition of PGJ(2) in the environment of infected intestinal epithelial cells could reduce HIV-1 transcription. |
Databáze: | OpenAIRE |
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