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Reversible Inhibition of Keratinocyte Thymidine Incorporation by the Calmodulin Antagonist, W‐7
Author(s) -
Hirokawa Masaki,
Hashimoto Yoshio,
Ohkuma Noritaka,
Mizumoto Toshihiro,
Iizuka Hajime
Publication year - 1990
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1990.tb01666.x
Subject(s) - calmodulin , keratinocyte , epidermis (zoology) , thymidine , antagonist , biology , microbiology and biotechnology , biochemistry , medicine , chemistry , in vitro , receptor , enzyme , anatomy
Although calmodulin has been suggested as an important regulator of keratinocyte proliferation, its precise role remains unknown. We employed a calmodulin antagonist, N‐(6‐aminohexyl)‐5‐chloro‐1‐naphthalenesulfonamide (W‐7), to examine the role of calmodulin on keratinocyte proliferation. N‐(6‐aminohexyl)‐1‐naphthalenesulfonamide (W‐5), a chlorine‐deficient analogue of W‐7 with little anti‐calmodulin activity, was used as the control. W‐7 markedly inhibited thymidine incorporation of pig epidermis at concentrations close to its anti‐calmodulin activity; W‐5 had no effect on the thymidine incorporation. The inhibitory effect of W‐7 was reversible; the removal of W‐7 from the incubation medium resulted in the reinitiation of the thymidine incorporation, suggesting that W‐7 is not a cytotoxic agent. These results are consistent with the view that calmodulin is an essential regulator of keratinocyte proliferation. The epidermal beta‐adrenergic response, which is decreased in various hyperproliferative epidermal abnormalities, was increased in W‐7‐treated hypoproliferative epidermis. The epidermal SOD activity, which is also decreased in the hyperproliferative epidermis, however, was not affected by the W‐7 treatment.