| Brain and muscle Arnt-like protein-1 (BMAL1) controls circadian cell proliferation and susceptibility to UVB-induced DNA damage in the epidermis. | |
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MedLine Citation:
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PMID: 22753467 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The role of the circadian clock in skin and the identity of genes participating in its chronobiology remain largely unknown, leading us to define the circadian transcriptome of mouse skin at two different stages of the hair cycle, telogen and anagen. The circadian transcriptomes of telogen and anagen skin are largely distinct, with the former dominated by genes involved in cell proliferation and metabolism. The expression of many metabolic genes is antiphasic to cell cycle-related genes, the former peaking during the day and the latter at night. Consistently, accumulation of reactive oxygen species, a byproduct of oxidative phosphorylation, and S-phase are antiphasic to each other in telogen skin. Furthermore, the circadian variation in S-phase is controlled by BMAL1 intrinsic to keratinocytes, because keratinocyte-specific deletion of Bmal1 obliterates time-of-day-dependent synchronicity of cell division in the epidermis leading to a constitutively elevated cell proliferation. In agreement with higher cellular susceptibility to UV-induced DNA damage during S-phase, we found that mice are most sensitive to UVB-induced DNA damage in the epidermis at night. Because in the human epidermis maximum numbers of keratinocytes go through S-phase in the late afternoon, we speculate that in humans the circadian clock imposes regulation of epidermal cell proliferation so that skin is at a particularly vulnerable stage during times of maximum UV exposure, thus contributing to the high incidence of human skin cancers. |
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Authors:
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Mikhail Geyfman; Vivek Kumar; Qiang Liu; Rolando Ruiz; William Gordon; Francisco Espitia; Eric Cam; Sarah E Millar; Padhraic Smyth; Alexander Ihler; Joseph S Takahashi; Bogi Andersen |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2012-07-02 |
Journal Detail:
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Title: Proceedings of the National Academy of Sciences of the United States of America Volume: 109 ISSN: 1091-6490 ISO Abbreviation: Proc. Natl. Acad. Sci. U.S.A. Publication Date: 2012 Jul |
Date Detail:
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Created Date: 2012-07-18 Completed Date: 2012-10-11 Revised Date: 2013-04-15 |
Medline Journal Info:
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Nlm Unique ID: 7505876 Medline TA: Proc Natl Acad Sci U S A Country: United States |
Other Details:
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Languages: eng Pagination: 11758-63 Citation Subset: IM |
Affiliation:
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Department of Biological Chemistry, University of California, Irvine, CA 92697, USA. |
| Data Bank Information | |
Bank Name/Acc. No.:
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GEO/GSE38625 |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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ARNTL Transcription Factors
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genetics,
metabolism* Animals Bromodeoxyuridine Cell Cycle / physiology Cell Proliferation* Circadian Rhythm / genetics*, physiology Colchicine DNA Damage / genetics*, physiology Enzyme-Linked Immunosorbent Assay Epidermis / cytology*, radiation effects Immunohistochemistry Male Metabolic Networks and Pathways / genetics*, physiology Mice Mice, Inbred C57BL Microarray Analysis Polymerase Chain Reaction Transcriptome / genetics*, physiology Ultraviolet Rays / adverse effects |
| Grant Support | |
ID/Acronym/Agency:
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AR56439/AR/NIAMS NIH HHS; F32 DA024556/DA/NIDA NIH HHS; T32-HD60555/HD/NICHD NIH HHS; UL1 TR000153/TR/NCATS NIH HHS; //Howard Hughes Medical Institute |
| Chemical | |
Reg. No./Substance:
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0/ARNTL Transcription Factors; 0/Arntl protein, mouse; 59-14-3/Bromodeoxyuridine; 64-86-8/Colchicine |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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