• Young-Suk Kim, Kyung-San Min, Hae-Doo Lee, Hyo-Won Oh, and Eun-Cheol Kim.
• Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University, Iksan, South Korea.
• J Endod. 2010 Apr 1; 36 (4): 636-41.

IntroductionAlthough cytokines stimulate prostaglandin E(2) (PGE(2)) production and cyclooxygenase-2 (COX-2) gene expression in human dental pulp cells (HDPCs), the involvement of cytosolic phospholipase A(2) (cPLA(2)) has not been assessed. The purpose of this study was to examine the role of cPLA(2) on the regulation of proinflammatory cytokine-stimulated genes associated with osteoclast differentiation or bone resorption.MethodsTumor necrosis factor-alpha (TNF-alpha) and interleukin-1alpha (IL-1alpha)-induced COX-2 and receptor activator of nuclear factor kappa B ligand (RANKL) mRNA and protein expression in the HDPCs was determined by using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. PGE(2) release and osteoclast-related gene expression were measured by enzyme-linked immunosorbent assay and RT-PCR.ResultsStimulation with TNF-alpha and IL-1alpha synergistically increased levels of COX-2 as well as RANKL mRNA and protein expression. Osteoclast markers (macrophage colony-stimulating factor [M-CSF], matrix metalloproteinase-9 [MMP-9], and tartrate-resistant acid phosphatase [TRAP]) and osteolysis regulating cytokines or osteoclastogenic cytokines (IL-6, IL-11, and Il-17) were up-regulated in HDPCs after IL-1alpha and TNF-alpha treatment. A cPLA(2) inhibitor attenuated both the cytokine-stimulated PGE(2) release as well as changes in osteoclast differentiation-related genes like RANKL.ConclusionsThese results suggest that cPLA(2) is involved in inflammatory cytokine-induced osteoclastogenic gene expression and consequent damage or destruction.Copyright (c) 2010 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.

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