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UV irradiation increases ROS production via PKCδ signaling in primary murine fibroblasts
Author(s) -
Bossi Orit,
Gartsbein Marina,
Leitges Michael,
Kuroki Toshio,
Grossman Shlomo,
Tennenbaum Tamar
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21817
Subject(s) - photoaging , protein kinase c , skin aging , microbiology and biotechnology , reactive oxygen species , senescence , chemistry , downregulation and upregulation , skin cancer , cancer research , signal transduction , biology , biochemistry , medicine , cancer , dermatology , genetics , gene
Abstract Ultraviolet (UV) irradiation is a major environmental factor responsible for a high incidence of premature skin aging, referred to as photoaging, as well as skin cancer and melanoma. UVA irradiation represents 90% of the solar UV light reaching the earth's surface, and yet the mechanisms by which it exerts its biological effects are not clear. UVA penetrates into the skin tissue, reaching the basal layers of the active dividing cells and, therefore, the contribution of UVA to skin damage may be significant. The majority of UVA energy is absorbed by unidentified photosensitizers in the cells which are postulated to generate reactive oxygen species (ROS). It has been believed that both chronological aging and photoaging share the same molecular features and, as such, it is very common to utilize UV irradiation for induction of skin aging. To determine the involvement of protein kinase isoforms in chronological aging and photoaging, we utilized in vitro aging model systems of primary murine fibroblasts and primary fibroblasts isolated from PKC null mice. We show for the first time distinct involvement of PKC isoforms PKCδ and PKCα in photoaging versus cellular senescence. While chronological aging is accompanied by overexpression and activation of PKCα, UV irradiation and ROS production are associated with photoaging accompanied by PKCδ downregulation and nuclear translocation. J. Cell. Biochem. 105: 194–207, 2008. © 2008 Wiley‐Liss, Inc.