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Increased expression of 14-3-3varepsilon protein in intrinsically aged and photoaged human skin in vivo

Cited 10 time in Web of Science Cited 10 time in Scopus
Authors

Choi, K. C.; Lee, S.; Kwak, S. Y.; Kim, M. S.; Choi, H. K.; Kim, K. H.; Chung, J. H.; Park, S. H.

Issue Date
2005-05-13
Publisher
Elsevier
Citation
Mech Ageing Dev. 2005 Jun-Jul;126(6-7):629-36. Epub 2005 Jan 21.
Keywords
14-3-3 Proteins/*biosynthesisAdolescentAdultAgedDermis/*metabolism/pathologyFemaleHumansMaleMiddle AgedSkin Aging/pathology/*physiology/radiation effectsUltraviolet Rays/adverse effects
Abstract
Skin aging is a complicated process associated with the passage of time and environmental exposure, especially to UV light. This aging phenomenon is related to alterations in various cellular mechanisms, such as changes in apoptosis, perturbations to cellular signaling, and an increased genetic instability. In this study, we investigated changes of proteins involved in intrinsic aging by the proteomic analysis of human sun-protected (upper inner arm) young and aged dermis. One of the proteins upregulated in aged dermis was identified as 14-3-3epsilon. This protein is an isoform of 14-3-3 protein, which is involved in cellular processes like signal transduction, cell cycle arrest, and apoptosis. 14-3-3epsilon is consistently found to be upregulated in the sun-protected dermis of aged skin, by Western blotting and immunohistochemical staining. In addition, we demonstrate that the expression of 14-3-3epsilon is further upregulated in the sun-exposed (photodamaged) dermis, and that the UV irradiation of young skin significantly upregulates 14-3-3epsilon in vivo. Our results suggest the possibility that the cellular processes related to 14-3-3epsilon protein play an important role in the photoaging and intrinsic aging of human skin.
ISSN
0047-6374 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15888315

https://hdl.handle.net/10371/22646
DOI
https://doi.org/10.1016/j.mad.2004.11.013
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