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Functional changes induced by chronic UVA irradiation to cultured human dermal fibroblasts
Author(s) -
Naru E.,
Suzuki T.,
Moriyama M.,
Inomata K.,
Hayashi A.,
Arakane K.,
Kaji K.
Publication year - 2005
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2005.06964.x
Subject(s) - fibroblast , irradiation , matrix metalloproteinase , ageing , in vivo , extracellular matrix , in vitro , human skin , extracellular , dermal fibroblast , chemistry , microbiology and biotechnology , biology , biochemistry , genetics , physics , nuclear physics
Summary Ultraviolet (UV) irradiation induces damage of the skin, and in particular, photoageing is known to be the result of chronic UV irradiation. Many investigations have attempted to clarify the mechanisms of photoageing induced by chronic UVA irradiation, but consensus has not been achieved yet by in vivo experiments, mostly due to differences among UV sources and animals used for experiments. In vitro experiments have shown that a single exposure to UVA irradiation causes overexpression of matrix metalloproteinases and denaturation of collagen, but the mechanisms of the photoageing effects of chronic UVA irradiation are still unclear. To examine the effects of chronic UVA irradiation, we used an in vitro fibroblast cellular ageing system as a model of photoageing. Chronic UVA irradiation of normal human fibroblasts induced shortening of the cellular life span and an increase of cellular diameter, in parallel with expression of senescence‐associated β‐galactosidase. Extracellular degradation enzyme, matrix metalloproteinase 1 (MMP‐1) was overexpressed after repeated UVA irradiation, but tissue inhibitor of metalloproteinase 1 (TIMP‐1) expression was hardly changed by chronic UVA irradiation. We conclude that chronic UVA irradiation of normal human fibroblasts induces cellular functional changes, leading to accelerated cellular ageing and MMP‐1 overexpression.

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