PMID- 20307736
OWN - NLM
STAT- MEDLINE
DCOM- 20100618
LR  - 20131121
IS  - 1878-3554 (Electronic)
IS  - 0099-2399 (Linking)
VI  - 36
IP  - 4
DP  - 2010 Apr
TI  - Effect of cytosolic phospholipase A2 on proinflammatory cytokine-induced bone 
      resorptive genes including receptor activator of nuclear factor kappa B ligand in 
      human dental pulp cells.
PG  - 636-41
LID - 10.1016/j.joen.2009.12.009 [doi]
AB  - INTRODUCTION: Although 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. METHODS: Tumor 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. 
      RESULTS: Stimulation 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. CONCLUSIONS: 
      These results suggest that cPLA(2) is involved in inflammatory cytokine-induced 
      osteoclastogenic gene expression and consequent damage or destruction.
CI  - Copyright (c) 2010 American Association of Endodontists. Published by Elsevier 
      Inc. All rights reserved.
FAU - Kim, Young-Suk
AU  - Kim YS
AD  - Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang 
      University, Iksan, South Korea.
FAU - Min, Kyung-San
AU  - Min KS
FAU - Lee, Hae-Doo
AU  - Lee HD
FAU - Oh, Hyo-Won
AU  - Oh HW
FAU - Kim, Eun-Cheol
AU  - Kim EC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Endod
JT  - Journal of endodontics
JID - 7511484
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1alpha)
RN  - 0 (RANK Ligand)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.13.11.34 (Arachidonate 5-Lipoxygenase)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 3.1.1.4 (Phospholipases A2, Cytosolic)
RN  - K7Q1JQR04M (Dinoprostone)
MH  - Arachidonate 5-Lipoxygenase/biosynthesis
MH  - Blotting, Western
MH  - Bone Resorption/*enzymology/*genetics
MH  - Cell Differentiation/genetics
MH  - Cell Line, Transformed
MH  - Cyclooxygenase 2/biosynthesis/genetics
MH  - Dental Pulp/cytology/*enzymology
MH  - Dinoprostone/biosynthesis/genetics
MH  - Enzyme Induction/drug effects
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - Interleukin-1alpha/pharmacology
MH  - Osteoclasts/cytology/drug effects/enzymology
MH  - Phospholipases A2, Cytosolic/antagonists & inhibitors/*metabolism
MH  - RANK Ligand/*biosynthesis/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Up-Regulation
EDAT- 2010/03/24 06:00
MHDA- 2010/06/19 06:00
CRDT- 2010/03/24 06:00
PHST- 2009/09/22 00:00 [received]
PHST- 2009/12/08 00:00 [revised]
PHST- 2009/12/12 00:00 [accepted]
PHST- 2010/03/24 06:00 [entrez]
PHST- 2010/03/24 06:00 [pubmed]
PHST- 2010/06/19 06:00 [medline]
AID - S0099-2399(09)01061-9 [pii]
AID - 10.1016/j.joen.2009.12.009 [doi]
PST - ppublish
SO  - J Endod. 2010 Apr;36(4):636-41. doi: 10.1016/j.joen.2009.12.009.