Sphingosine-1-phosphate signaling in human submandibular cells

J. Seo; N. Y. Koo; W. Y. Choi; J. A. Kang; J. H. Min; S. H. Jo; S. J. Lee; S. B. Oh; J. S. Kim; J. H. Lee; S. Y. Choi; K. Park

doi:10.1177/0022034510376044

Sphingosine-1-phosphate signaling in human submandibular cells

J. Seo
, N. Y. Koo
, W. Y. Choi
, J. A. Kang
, J. H. Min
, S. H. Jo
, S. J. Lee
, S. B. Oh
, J. S. Kim
, J. H. Lee
, S. Y. Choi
, K. Park

Department of Brain Sciences

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

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 Sjögren'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 ([Ca ²⁺]_i), which was inhibited by pre-treatment with U73122 or 2-aminoethoxydiphenyl 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 Ca²⁺ signaling and the apoptotic pathway in normal submandibular gland cells, which suggests in turn that S1P affects the progression of Sjögren's syndrome.

Original language	English
Pages (from-to)	1148-1153
Number of pages	6
Journal	Journal of Dental Research
Volume	89
Issue number	10
DOIs	https://doi.org/10.1177/0022034510376044
State	Published - Oct 2010

Bibliographical note

Funding Information:
This work was supported by the Korea Science & Engineering Foundation (grant R13–2008–008–01001–0) through the Oromaxillofacial Dysfunction Research Center for the Elderly at Seoul National University.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

intracellular calcium
receptor
sphingosine kinase
sphingosine-1-phosphate
submandibular gland

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10.1177/0022034510376044

Cite this

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title = "Sphingosine-1-phosphate signaling in human submandibular cells",

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 Sj{\"o}gren'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 ([Ca 2+]i), which was inhibited by pre-treatment with U73122 or 2-aminoethoxydiphenyl 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 Ca2+ signaling and the apoptotic pathway in normal submandibular gland cells, which suggests in turn that S1P affects the progression of Sj{\"o}gren's syndrome.",

keywords = "intracellular calcium, receptor, sphingosine kinase, sphingosine-1-phosphate, submandibular gland",

author = "J. Seo and Koo, \{N. Y.\} and Choi, \{W. Y.\} and Kang, \{J. A.\} and Min, \{J. H.\} and Jo, \{S. H.\} and Lee, \{S. J.\} and Oh, \{S. B.\} and Kim, \{J. S.\} and Lee, \{J. H.\} and Choi, \{S. Y.\} and K. Park",

note = "Funding Information: This work was supported by the Korea Science \& Engineering Foundation (grant R13–2008–008–01001–0) through the Oromaxillofacial Dysfunction Research Center for the Elderly at Seoul National University.",

year = "2010",

month = oct,

doi = "10.1177/0022034510376044",

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AU - Seo, J.

AU - Koo, N. Y.

AU - Choi, W. Y.

AU - Kang, J. A.

AU - Min, J. H.

AU - Jo, S. H.

AU - Lee, S. J.

AU - Oh, S. B.

AU - Kim, J. S.

AU - Lee, J. H.

AU - Choi, S. Y.

AU - Park, K.

N1 - Funding Information: This work was supported by the Korea Science & Engineering Foundation (grant R13–2008–008–01001–0) through the Oromaxillofacial Dysfunction Research Center for the Elderly at Seoul National University.

PY - 2010/10

Y1 - 2010/10

N2 - 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 Sjögren'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 ([Ca 2+]i), which was inhibited by pre-treatment with U73122 or 2-aminoethoxydiphenyl 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 Ca2+ signaling and the apoptotic pathway in normal submandibular gland cells, which suggests in turn that S1P affects the progression of Sjögren's syndrome.

AB - 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 Sjögren'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 ([Ca 2+]i), which was inhibited by pre-treatment with U73122 or 2-aminoethoxydiphenyl 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 Ca2+ signaling and the apoptotic pathway in normal submandibular gland cells, which suggests in turn that S1P affects the progression of Sjögren's syndrome.

KW - intracellular calcium

KW - receptor

KW - sphingosine kinase

KW - sphingosine-1-phosphate

KW - submandibular gland

UR - https://www.scopus.com/pages/publications/78049427228

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DO - 10.1177/0022034510376044

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SN - 0022-0345

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EP - 1153

JO - Journal of Dental Research

JF - Journal of Dental Research

IS - 10

ER -

Sphingosine-1-phosphate signaling in human submandibular cells

Abstract

Bibliographical note

UN SDGs

Keywords

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