Document Detail


Parameters of protection against ultraviolet radiation-induced skin cell damage.
MedLine Citation:
PMID:  19360745     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epidemiological and experimental evidence has supported the notion that solar ultraviolet (UV) radiation is the leading cause of skin cell damage and skin cancer. Non-melanoma skin cancer, one of the malignancies with the most rapidly increasing incidence, is suggested to be directly related to the total exposure to solar UV light. Over the past few years, the mechanisms of cellular responses to UV radiation have received unprecedented attention. Understanding how skin cells respond to UV radiation will undoubtedly help decipher what goes wrong in a variety of clinical skin disorders including skin cancer and will facilitate the development of novel therapeutic strategies. In the past decade, studies have established that UV radiation induces multifarious signal transduction pathways, some of which lead to apoptotic cell death, while others protect against this process. In this review, we summarize some of the most recent progresses regarding the involvement of multiple signal pathways in UV radiation-induced apoptosis in skin cells, especially in keratinocytes. These pathways include pro-apoptosis components such as MAPK, AMPK, and p53 as well as pro-survival components, namely, AKT and mTORC complexes.
Authors:
Cong Cao; Yinsheng Wan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  220     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-06-01     Completed Date:  2009-06-29     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  277-84     Citation Subset:  IM    
Affiliation:
Department of Molecular Microbiology and Immunology, Brown University, Providence, RI 02912, USA. cong_cao@brown.edu
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MeSH Terms
Descriptor/Qualifier:
Adenylate Kinase / metabolism
Animals
Apoptosis / physiology,  radiation effects
Enzyme Activation
Humans
Mitogen-Activated Protein Kinases / metabolism
Multiprotein Complexes / metabolism
Protein Kinases / metabolism
Protein Processing, Post-Translational
Proto-Oncogene Proteins c-akt / metabolism
Reactive Oxygen Species / metabolism
Signal Transduction / physiology
Skin* / pathology,  radiation effects
Skin Neoplasms / epidemiology,  prevention & control*
Tumor Suppressor Protein p53 / metabolism
Ultraviolet Rays / adverse effects*
Grant Support
ID/Acronym/Agency:
2 P20 RR018757-06/RR/NCRR NIH HHS; P20 RR016457/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Multiprotein Complexes; 0/Reactive Oxygen Species; 0/Tumor Suppressor Protein p53; EC 2.7.-/Protein Kinases; EC 2.7.1.-/mTOR protein; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.4.3/Adenylate Kinase

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


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