TY - JOUR
T1 - Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation
AU - Madson, Justin G.
AU - Lynch, David T.
AU - Tinkum, Kelsey L.
AU - Putta, Sumanth K.
AU - Hansen, Laura A.
N1 - Funding Information:
This publication was supported by the National Institutes of Health (grants P20 RR018759 and P20 RR017717-01 ) and by the State of Nebraska LB692. This investigation was conducted in a facility constructed with support from Research Facilities Improvement Program grant 1 CO6 RR17417-01 from the National Center for Research Resources, National Institutes of Health.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2006/10
Y1 - 2006/10
N2 - 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-κB and Comp1, including interleukin-1β, prostaglandinendoperoxidase 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.
AB - 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-κB and Comp1, including interleukin-1β, prostaglandinendoperoxidase 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.
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U2 - 10.2353/ajpath.2006.060082
DO - 10.2353/ajpath.2006.060082
M3 - Article
C2 - 17003495
AN - SCOPUS:34347211899
VL - 169
SP - 1402
EP - 1414
JO - American Journal of Pathology
JF - American Journal of Pathology
SN - 0002-9440
IS - 4
ER -