Document Detail


Signal transduction and HIV transcriptional activation after exposure to ultraviolet light and other DNA-damaging agents.
MedLine Citation:
PMID:  8760569     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Short wavelength (254 nm) ultraviolet light (UVC) radiation was much more potent in activating transcription of human immunodeficiency virus 1 (HIV) reporter genes stably integrated into the genomes of human and monkey cells than ionizing radiation (IR) from a 137Cs source at similarly cytotoxic doses. A similar differential was also observed when c-jun transcription levels were examined. However, these transcription levels do not correlate with activation of nuclear factor (NF)-kappa B and AP-1 measured by band-shift assays, i.e. both types of radiation produce similar increases in NF-kappa B and AP-1 activity, suggesting existence of additional levels of regulation during these responses. Because of the well-established involvement of cytoplasmic signaling pathways in the cellular response to tumor necrosis factor-alpha (TNF-alpha), UVC, and IR using other types of assays, the role of TNF-alpha in the UVC response of HIV and c-jun was investigated in our cell system. We demonstrate that UVC and TNF-alpha activate HIV gene expression in a synergistic fashion, suggesting that it is unlikely that TNF-alpha is involved in UVC activation of HIV transcription in stably transfected HeLa cells. Moreover, maximum TNF-alpha stimulation resulted in one order of magnitude lower levels of HIV expression than that observed after UVC exposure. We also observed an additive effect of UVC and TNF-alpha on c-jun steady-state mRNA levels, suggestive of a partial overlap in activation mechanism of c-jun by UVC and TNF-alpha; yet these responses are distinct to some extent. Our results indicate that the HIV, and to some extent also the c-jun, transcriptional responses to UVC are not the result of TNF-alpha stimulation and subsequent downstream cytoplasmic signaling events in HeLa cells. Additional levels of regulation that do not directly involve the NF-kappa B and AP-1 transcription factors, such as changes in chromatin structure associated with the UV repair process, may also be important for a full transcriptional response of HIV and c-jun to UVC. In addition to the new data, this report also summarizes our current views regarding UVC-induced activations of HIV gene expression in stably transfected cells.
Authors:
K Valerie; W S Laster; L Cheng; J C Kirkham; P Reavey; N B Kuemmere
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Photochemistry and photobiology     Volume:  64     ISSN:  0031-8655     ISO Abbreviation:  Photochem. Photobiol.     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1996-10-01     Completed Date:  1996-10-01     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0376425     Medline TA:  Photochem Photobiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  280-5     Citation Subset:  IM; X    
Affiliation:
Department of Radiation Oncology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0058, USA. kvalerie@gems.vcu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cercopithecus aethiops
DNA Damage*
DNA, Viral / genetics,  radiation effects*
Genes, Viral / radiation effects
HIV-1 / genetics,  radiation effects*
Hela Cells
Humans
Infrared Rays / adverse effects
Signal Transduction / radiation effects*
Transcriptional Activation / radiation effects*
Ultraviolet Rays / adverse effects*
Grant Support
ID/Acronym/Agency:
CA53199/CA/NCI NIH HHS; CA61945/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/DNA, Viral

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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