Abstract
Introduction
Vascular cell adhesion molecule (VCAM-1) plays a critical role in the inflammatory
processes by stimulating the recruitment, extravasation, and migration of leukocytes.
Its expression and regulation in the dental pulp is not well elucidated.
Methods
Primary dental pulp cells were exposed to prostaglandin E2 (PGE2), prostaglandin F2α (PGF2α), or interleukin 1β (IL-1β) with/without aspirin. VCAM-1 messenger RNA expression
was analyzed by reverse transcriptase–polymerase chain reaction. Soluble VCAM-1 (sVCAM-1)
in the culture medium was determined by enzyme-linked immunosorbent assay, and the
number of viable cells was estimated by (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium
bromide (MTT) assay.
Results
IL-1β induced VCAM-1 gene expression of pulp cells. IL-1β also stimulated sVCAM-1
production. The IL-1β–induced sVCAM-1 production was not inhibited but rather enhanced
by aspirin, a cyclooxygenase (COX) inhibitor. PGE2 and PGF2α decreased the VCAM-1 expression and sVCAM-1 production of pulp cells. U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene),
a mitogen-activated protein kinase kinase (MEK) inhibitor, attenuated IL-1β–induced
sVCAM-1 production. However, no marked cytotoxicity was noted in these experimental
conditions as analyzed by MTT assay.
Conclusions
IL-1β may be involved in the pulpal inflammatory processes via stimulation of VCAM-1
expression and sVCAM-1 production. This event is not mediated by COX activation and
prostanoid production but is associated with MEK signaling. PGE2 and PGF2α may potentially regulate inflammatory processes by the inhibition of VCAM-1.
Key Words
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Article info
Publication history
Published online: April 13, 2012
Footnotes
Supported by National Science Council (NSC), Taiwan, and Chang Gung Memorial Hospital (CMRP).
Identification
Copyright
© 2012 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.
