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Interleukin‐1 alpha derived from ultraviolet B‐exposed keratinocytes is associated with a decrease of endocytic collagen receptor Endo180
Author(s) -
Iwahashi Hiroyasu,
Kawashima Yoshihito,
Masaki Hitoshi
Publication year - 2020
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/phpp.12502
Subject(s) - internalization , extracellular matrix , fibroblast , keratinocyte , chemistry , flow cytometry , matrix metalloproteinase , receptor , microbiology and biotechnology , biology , biochemistry , in vitro
Background Endo180 contributes to the remodeling of the collagen fibers that comprise the dermal matrix due to the internalization of extracellular collagen fragments. In the sun‐exposed elder skin, an accumulation of collagen fragments was observed in the dermal matrix which was associated with a reduction in Endo180 in the dermal fibroblasts. This suggests that the loss of Endo180 results in the accumulation of collagen fragments in the surrounding fibroblasts and causes interference with dermal matrix remodeling via collagen fibers. The purpose of the study was to identify a mechanism by which ultraviolet B (UVB) exposure induces a loss of Endo 180 with a specific focus on the crosstalk between keratinocytes and fibroblasts. Methods Endo180 from normal human dermal fibroblasts, which were cultured with a conditioned medium (CM) of UVB‐exposed keratinocytes, was examined using mRNA expression, protein levels and collagen internalization by quantitative RT‐PCR, ELISA, and flow cytometry, respectively. Results Although UVB irradiation to fibroblasts failed to reduce Endo180, the CM of UVB‐exposed keratinocytes reduced Endo180 in the fibroblasts. Collagen internalization into the fibroblasts was decreased and was associated with a loss of Endo180. Among cytokines secreted from UVB‐exposed keratinocytes, IL‐1α solely reduced Endo180, and the reduction induced by the CM of UVB‐exposed keratinocytes was abolished by the presence of IL‐1RA. Conclusions These results indicate that a substance secreted from UVB‐exposed keratinocytes regulates Endo180 expression and that IL‐1α may play an important role in the maintenance of Endo180.