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Sphingosylphosphorylcholine stimulates contraction of fibroblast‐embedded collagen gel
Author(s) -
Suhr K.B.,
Tsuboi R.,
Ogawa H.
Publication year - 2000
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 - 10.1046/j.1365-2133.2000.03592.x
Subject(s) - pertussis toxin , fibroblast , staurosporine , contraction (grammar) , wound healing , signal transduction , ceramide , sphingosine , biochemistry , chemistry , protein kinase c , receptor , in vitro , biology , endocrinology , g protein , apoptosis , immunology
Sphingosylphosphorylcholine (SPC), a sphingolipid metabolite, has recently been reported to stimulate wound healing in an animal model. To clarify the mechanism of SPC on the healing process, we examined the effect of SPC on wound contraction using an in vitro model. A mixture of human dermal fibroblasts and porcine type I collagen in a serum‐free medium was gelled, and then separated from the well after a 12‐h incubation. Various reagents were applied to the medium, and its contractile activity was analysed by measuring the amount of contracted surface area. Among the sphingolipid metabolites, SPC and sphingosine‐1‐phosphate, but not sphingosine, C 2 ‐ceramide and C 6 ‐ceramide, stimulated collagen gel contraction. Maximal gel contraction, observed at 10 μmol L −1 of SPC, occurred as early as 1 h after the treatment and persisted for more than 48 h. The effect of SPC was not inhibited by pretreatment with antitransforming growth factor‐β or antiplatelet‐derived growth factor‐BB antibodies. Among the various signal transduction inhibitors, pertussis toxin, staurosporine and H7 were found to inhibit the action of SPC, whereas genistein and tyrphostin A47 were not, suggesting that fibroblast contraction induced by SPC is mediated by a trimeric guanosine triphosphate ‐binding protein (G protein)‐coupled receptor and protein kinase. Our findings imply that the effect of SPC as a healing stimulant might be due in part to stimulation of fibroblast contraction in granulation tissue.