Premium
Intracellular Signaling Mechanisms Involved in the Biological Effects of the Xanthophyll Carotenoid Astaxanthin to Prevent the Photo‐aging of the Skin in a Reactive Oxygen Species Depletion‐independent Manner: The Key Role of Mitogen and Stress‐activated Protein Kinase 1
Author(s) -
Imokawa Genji
Publication year - 2018
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.13034
Subject(s) - microphthalmia associated transcription factor , microbiology and biotechnology , transcription factor , xanthophyll , creb , signal transduction , intracellular , reactive oxygen species , astaxanthin , biology , p38 mitogen activated protein kinases , chemistry , mapk/erk pathway , biochemistry , carotenoid , gene
Abstract In the first review, we summarized the biological effects of the xanthophyll carotenoid astaxanthin ( AX ) to prevent UV ‐induced cutaneous inflammation, abnormal keratinization, pigmentation, and wrinkling in a manner independent of the depletion of reactive oxygen species. In this manuscript, we review what is known about the intracellular signaling mechanisms that are involved in those effects in keratinocytes and in melanocytes. Our research has characterized the intracellular stress signaling mechanism(s) that are involved in the up‐regulated expression of genes encoding cyclooxygenase ( COX 2), interleukin ( IL )‐8, granulocyte macrophage colony stimulatory factor ( GM ‐ CSF ), and transglutaminase ( TG ase)1 in UVB ‐exposed keratinocytes as well as in the stimulated transcription and/or translation of melanogenic factors, including microphthalmia‐associated transcription factor ( MITF ), in stem cell factor ( SCF )‐treated melanocytes. The results reveal that while the expression of COX 2, IL ‐8, GM ‐ CSF , and TG ase1 stimulated by UVB is due to effects primarily via the NF κB pathway, that stimulation can be abrogated by specifically interrupting the p38/ MSK 1/ NF κBp65Ser276 axis. Further, the stimulation of melanogenesis by SCF can be inhibited by disrupting the phosphorylation of MSK 1 via the p38, MSK 1, CREB , and MITF axis. The sum of these findings provides new evidence for the interruption of ROS depletion independent‐signaling by antioxidants.