Document Detail


Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation.
MedLine Citation:
PMID:  17003495     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Exposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer.
Authors:
Justin G Madson; David T Lynch; Kelsey L Tinkum; Sumanth K Putta; Laura A Hansen
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of pathology     Volume:  169     ISSN:  0002-9440     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2006 Oct 
Date Detail:
Created Date:  2006-09-27     Completed Date:  2006-11-24     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1402-14     Citation Subset:  AIM; IM    
Affiliation:
Department of Biomedical Sciences, School of Medicine, Creighton University, 2500 California Plaza, Omaha, NE 68178, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / genetics
Benzothiazoles / pharmacology
Binding Sites
Cell Proliferation
Chemokines / genetics
Cyclooxygenase 2 / genetics
Female
Gene Expression Regulation*
Interleukin-1beta / genetics
Mice
Mice, Inbred Strains
Oncogene Proteins v-erbB / antagonists & inhibitors,  genetics,  physiology*
Protein Kinase Inhibitors / pharmacology
Radiodermatitis / genetics*,  metabolism
Skin / metabolism,  radiation effects*
Skin Neoplasms / etiology*,  genetics
Transcription Factors / metabolism
Transcription, Genetic / radiation effects
Tyrphostins / pharmacology
Ultraviolet Rays*
Grant Support
ID/Acronym/Agency:
1 C06 RR17417-01/RR/NCRR NIH HHS; P20 RR017717-01/RR/NCRR NIH HHS; P20 RR018759/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Benzothiazoles; 0/Chemokines; 0/Interleukin-1beta; 0/Oncogene Proteins v-erbB; 0/Protein Kinase Inhibitors; 0/Transcription Factors; 0/Tyrphostins; 0/tyrphostin AG825; EC 1.14.99.1/Cyclooxygenase 2
Comments/Corrections

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