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Sphingosine-1-phosphate signaling in human submandibular cells

Cited 6 time in Web of Science Cited 7 time in Scopus
Authors
Seo, J.; Koo, N.-Y.; Choi, W.-Y.; Kang, J.-A.; Jo, S.-H.; Oh, S.-B.; Lee, J.-H.; Park, K.; Choi, S.-Y.; Kim, J.-S.; Lee, S.J.; Min, J.H.
Issue Date
2010
Publisher
SAGE Publications
Citation
Journal of Dental Research, Vol.89, 10, pp.1148-1153
Keywords
intracellular calciumsphingosine kinasereceptorsphingosine-1-phosphatesubmandibular gland
Description
A supplemental appendix to this article is published electronically only at http://jdr.sagepub.com/supplemental.
Abstract
Sphingosine-1-phosphate (S1P) is a significant lipid messenger modulating many physiological responses. S1P plays a critical role in autoimmune disease and is suggested to be involved in Sjogren`s syndrome pathology. However, the mechanism of S1P signaling in salivary glands is unclear. Here we studied the effects of S1P on normal human submandibular gland cells. S1P increased levels of the intracellular Ca2+ concentration ([Ca2+]i), which was inhibited by pre-treatment with U73122 2-minoethoxydiphenyl borate (2-APB). Pre-treated S1P did not inhibit subsequent carbachol-induced [Ca2+]i increase, which suggests that S1P and muscarinic signaling are independent of each other. S1P1, S1P2, and S1P3 receptors SphK1 and SphK2 were commonly expressed in human salivary gland cells. S1P, but not carbachol, induces the expression of interleukin-6 and Fas. Our results suggest that S1P triggers Ca 2+ signaling and the apoptotic pathway in normal submandibular gland cells, which suggests in turn that S1P affects the progression of Sjogren`s syndrome. (C) 2010 International & American Associations for Dental Research.
ISSN
0022-0345
Language
English
URI
https://hdl.handle.net/10371/80920
DOI
https://doi.org/10.1177/0022034510376044
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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