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Covalent binding of retinoic acid to cytokeratins 16 and 10 accompanies its action in mouse skin tissues
Author(s) -
Takahashi Noriko,
Ohba Toshihiro,
Imai Masahiko,
Sasaki Yuichi,
Kumaoka Takaya,
Takahashi Katsuhiko,
Fujiu Yasunori
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.951.5
Subject(s) - retinoic acid , cytokeratin , hairless , keratin , in vivo , microbiology and biotechnology , receptor , chemistry , biology , biochemistry , immunohistochemistry , immunology , gene , genetics
Retinoic acid (RA) has various biological effects in mammalian cells and tissues. In epidermal cells, RA is an inhibitor of differentiation to the squamous phenotype. The molecular mechanisms underlying the primary effects of RA are mediated by RA nuclear receptors as well as by retinoylation (acylation by RA), a protein post‐translational modification. To understand those components arising from the actions of RA via RA nuclear receptors versus retinoylation on epidermal cells, we examined the effects of topical RA treatment on the skin of hairless mice. RA binding proteins were determined by immunoblotting using anti‐RA antibodies and identified by MALDI‐TOF‐MS. RA increased epidermal thickness and decreased matrix metalloprotease and hyaluronidase activities in mouse skin tissues. We identified eight RA‐binding proteins that were increased by topical RA treatment. Three of these proteins were identified as cytokeratin 10, cytokeratin 16 and serum albumin. These results raise the possibility that RA binding to cytokeratins in vivo may be involved in effects of RA on keratinocytes of mouse skins. This investigation was supported in part by the Ministry of Education, Culture, Sports, Science and Technology, Japan and the Open Research Center Project.