J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on January 1, 2003

Papers In Press, published online ahead of print October 1, 2002
J. Lipid Res., doi:10.1194/jlr.M200225-JLR200
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Submitted on June 12, 2002
Revised on August 20, 2002
Accepted on October 1, 2002

Sphingosylphosphorylcholine levels are significantly increased in the stratum corneum of patients with a topic dermatitis: Physiological and functional relevance of sphingomyelin deacylase to the ceramide deficiency

Reiko Okamoto, Junko Arikawa, Mutsumi Ishibashi, Makoto Kawashima, Yutaka Takagi, and Genji Imokawa

Biological Science Laboratories, Kao Corporation, Tochigi 321-3497

Corresponding Author: imokawag{at}dream.ocn.ne.jp

To clarify the physiological and functional relevance of sphingomyelin (SM) deacylase to the ceramide deficiency seen in atopic dermatitis (AD), we developed a new highly sensitive method to measure the metabolic intermediate sphingosylphosphorylcholine (SPC) that accumulates in the stratum corneum and we quantitated amounts of SPC per mg stratum corneum at the nanomolar level. SPC in intercellular lipids extracted from stratum corneum that had been tape-stripped 3 times was reacted with [14C]-acetic anhydride to yield 14C-C2-SM which was then analyzed by thin layer chromatography and was quantitated using a imaging analyzer. In both the lesional and non-lesional stratum corneum obtained from patients with AD, there was a significant increase in the content of SPC over that present in the stratum corneum of healthy control subjects. There was a reciprocal relationship between increases in SPC and decreases in ceramide levels of stratum corneum obtained from healthy controls, and from lesional and non-lesional skin from patients with AD. Comparison with other sphingolipids present in the stratum corneum demonstrated that there is a significant positive correlation (n = 30, r = 0.70, p < 0.001) between SPC and glucosylsphingosine, another lysosphingolipid derived from glucosylceramide by another novel epidermal enzyme, termed glucosylceramide deacylase. In contrast, there was no correlation between SPC and sphingosine, a degradative product generated from ceramide by ceramidase. These findings strongly suggest the physiological relevance of SM deacylase function in vivo to the ceramide deficiency found in the skin of patients with AD.


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