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Sphingosine-1-phosphate inhibits interleukin-1β-induced inflammation in human articular chondrocytes.
Int J Mol Med. 2012 Dec; 30(6):1451-8.IJ

Abstract

Sphingosine-1-phosphate (S1P) is a pluripotent lipid mediator that transmits signals through a family of G-protein-coupled receptors (GPCRs) to control diverse biological processes including inflammation and wound-healing. In this study, a novel biological activity of S1P in articular chondrocytes was identified. Human primary chondrocytes were cultured in a monolayer. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were performed to detect genes and proteins involved in inflammation and cartilage degradation when human primary chondrocytes were stimulated by interleukin (IL)-1β. Matrix metalloproteinase (MMP)-2 and MMP-9 activity was evaluated by gelatin zymography. Glycosaminoglycan (GAG) degradation was evaluated using the dimethylene blue method. Prostaglandin E2 (PGE2) was measured by enzyme-linked immunosorbent assay (ELISA). By using the S1P1 receptor agonist and antagonist, we discovered the key role played by S1P1 in the S1P-dependent inhibition of IL-1β-induced inflammation in human chondrocytes. S1P dose-dependently inhibited IL-1β-induced NF-κB p65, cyclooxygenase (COX)-2, MMP-1, MMP-3, MMP-13 and MMP-14 mRNA expression in human chondrocytes and IL-1β-induced PGE2 synthesis and GAG degradation in human cartilage explants. W146, a known S1P1 receptor antagonist, inhibited the active form of NF-κB p65 and COX-2 expression induced by IL-1β. The anti-inflammatory action of the S1P1 receptor agonist SEW2871 was similar to that of S1P. This study demonstrates that S1P has anti-inflammatory effects on chondrocytes via the S1P1 receptor. Our data suggest that targeting S1P and S1P1 may be a potential therapy for arthritis.

Authors+Show Affiliations

Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Jeonbuk 561-756, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22992945

Citation

Moon, Myung-Hee, et al. "Sphingosine-1-phosphate Inhibits Interleukin-1β-induced Inflammation in Human Articular Chondrocytes." International Journal of Molecular Medicine, vol. 30, no. 6, 2012, pp. 1451-8.
Moon MH, Jeong JK, Lee YJ, et al. Sphingosine-1-phosphate inhibits interleukin-1β-induced inflammation in human articular chondrocytes. Int J Mol Med. 2012;30(6):1451-8.
Moon, M. H., Jeong, J. K., Lee, Y. J., Seol, J. W., & Park, S. Y. (2012). Sphingosine-1-phosphate inhibits interleukin-1β-induced inflammation in human articular chondrocytes. International Journal of Molecular Medicine, 30(6), 1451-8. https://doi.org/10.3892/ijmm.2012.1135
Moon MH, et al. Sphingosine-1-phosphate Inhibits Interleukin-1β-induced Inflammation in Human Articular Chondrocytes. Int J Mol Med. 2012;30(6):1451-8. PubMed PMID: 22992945.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sphingosine-1-phosphate inhibits interleukin-1β-induced inflammation in human articular chondrocytes. AU - Moon,Myung-Hee, AU - Jeong,Jae-Kyo, AU - Lee,You-Jin, AU - Seol,Jae-Won, AU - Park,Sang-Youel, Y1 - 2012/09/19/ PY - 2012/06/24/received PY - 2012/07/26/accepted PY - 2012/9/21/entrez PY - 2012/9/21/pubmed PY - 2013/5/29/medline SP - 1451 EP - 8 JF - International journal of molecular medicine JO - Int. J. Mol. Med. VL - 30 IS - 6 N2 - Sphingosine-1-phosphate (S1P) is a pluripotent lipid mediator that transmits signals through a family of G-protein-coupled receptors (GPCRs) to control diverse biological processes including inflammation and wound-healing. In this study, a novel biological activity of S1P in articular chondrocytes was identified. Human primary chondrocytes were cultured in a monolayer. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were performed to detect genes and proteins involved in inflammation and cartilage degradation when human primary chondrocytes were stimulated by interleukin (IL)-1β. Matrix metalloproteinase (MMP)-2 and MMP-9 activity was evaluated by gelatin zymography. Glycosaminoglycan (GAG) degradation was evaluated using the dimethylene blue method. Prostaglandin E2 (PGE2) was measured by enzyme-linked immunosorbent assay (ELISA). By using the S1P1 receptor agonist and antagonist, we discovered the key role played by S1P1 in the S1P-dependent inhibition of IL-1β-induced inflammation in human chondrocytes. S1P dose-dependently inhibited IL-1β-induced NF-κB p65, cyclooxygenase (COX)-2, MMP-1, MMP-3, MMP-13 and MMP-14 mRNA expression in human chondrocytes and IL-1β-induced PGE2 synthesis and GAG degradation in human cartilage explants. W146, a known S1P1 receptor antagonist, inhibited the active form of NF-κB p65 and COX-2 expression induced by IL-1β. The anti-inflammatory action of the S1P1 receptor agonist SEW2871 was similar to that of S1P. This study demonstrates that S1P has anti-inflammatory effects on chondrocytes via the S1P1 receptor. Our data suggest that targeting S1P and S1P1 may be a potential therapy for arthritis. SN - 1791-244X UR - https://www.unboundmedicine.com/medline/citation/22992945/Sphingosine_1_phosphate_inhibits_interleukin_1β_induced_inflammation_in_human_articular_chondrocytes_ L2 - http://www.spandidos-publications.com/ijmm/30/6/1451 DB - PRIME DP - Unbound Medicine ER -