Regulation of vascular cell adhesion molecule-1 in dental pulp cells by interleukin-1β

The role of prostanoids

Mei Chi Chang, Li Deh Lin, Jenny Zwei-Ching Chang, Chiung Fang Huang, Fu Hsiung Chuang, Jang Jaer Lee, Po Yuan Jeng, Tong Mei Wang, Jiiang Huei Jeng

Research output: Contribution to journalArticle

11 Citations (Scopus)

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 E 2 (PGE 2), prostaglandin F (PGF ), 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. PGE 2 and PGF 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. PGE 2 and PGF may potentially regulate inflammatory processes by the inhibition of VCAM-1.

Original languageEnglish
Pages (from-to)774-779
Number of pages6
JournalJournal of Endodontics
Volume38
Issue number6
DOIs
Publication statusPublished - Jun 2012

Fingerprint

Dental Pulp
Vascular Cell Adhesion Molecule-1
Interleukin-1
Prostaglandins
Mitogen-Activated Protein Kinase Kinases
Prostaglandins F
Prostaglandins E
Aspirin
Cyclooxygenase Inhibitors
Deciduous Tooth
Prostaglandin-Endoperoxide Synthases
Reverse Transcriptase Polymerase Chain Reaction
Culture Media

Keywords

  • Dental pulp cells
  • inflammation
  • interleukin-1β
  • prostanoids
  • vascular cell adhesion molecule

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Regulation of vascular cell adhesion molecule-1 in dental pulp cells by interleukin-1β : The role of prostanoids. / Chang, Mei Chi; Lin, Li Deh; Zwei-Ching Chang, Jenny; Huang, Chiung Fang; Chuang, Fu Hsiung; Lee, Jang Jaer; Jeng, Po Yuan; Wang, Tong Mei; Jeng, Jiiang Huei.

In: Journal of Endodontics, Vol. 38, No. 6, 06.2012, p. 774-779.

Research output: Contribution to journalArticle

Chang, MC, Lin, LD, Zwei-Ching Chang, J, Huang, CF, Chuang, FH, Lee, JJ, Jeng, PY, Wang, TM & Jeng, JH 2012, 'Regulation of vascular cell adhesion molecule-1 in dental pulp cells by interleukin-1β: The role of prostanoids', Journal of Endodontics, vol. 38, no. 6, pp. 774-779. https://doi.org/10.1016/j.joen.2012.02.030
Chang, Mei Chi ; Lin, Li Deh ; Zwei-Ching Chang, Jenny ; Huang, Chiung Fang ; Chuang, Fu Hsiung ; Lee, Jang Jaer ; Jeng, Po Yuan ; Wang, Tong Mei ; Jeng, Jiiang Huei. / Regulation of vascular cell adhesion molecule-1 in dental pulp cells by interleukin-1β : The role of prostanoids. In: Journal of Endodontics. 2012 ; Vol. 38, No. 6. pp. 774-779.
@article{27510463aa7040528dd9f4bd5cac4a69,
title = "Regulation of vascular cell adhesion molecule-1 in dental pulp cells by interleukin-1β: The role of prostanoids",
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 E 2 (PGE 2), prostaglandin F 2α (PGF 2α), 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. PGE 2 and PGF 2α 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. PGE 2 and PGF 2α may potentially regulate inflammatory processes by the inhibition of VCAM-1.",
keywords = "Dental pulp cells, inflammation, interleukin-1β, prostanoids, vascular cell adhesion molecule",
author = "Chang, {Mei Chi} and Lin, {Li Deh} and {Zwei-Ching Chang}, Jenny and Huang, {Chiung Fang} and Chuang, {Fu Hsiung} and Lee, {Jang Jaer} and Jeng, {Po Yuan} and Wang, {Tong Mei} and Jeng, {Jiiang Huei}",
year = "2012",
month = "6",
doi = "10.1016/j.joen.2012.02.030",
language = "English",
volume = "38",
pages = "774--779",
journal = "Journal of Endodontics",
issn = "0099-2399",
publisher = "Elsevier Inc.",
number = "6",

}

TY - JOUR

T1 - Regulation of vascular cell adhesion molecule-1 in dental pulp cells by interleukin-1β

T2 - The role of prostanoids

AU - Chang, Mei Chi

AU - Lin, Li Deh

AU - Zwei-Ching Chang, Jenny

AU - Huang, Chiung Fang

AU - Chuang, Fu Hsiung

AU - Lee, Jang Jaer

AU - Jeng, Po Yuan

AU - Wang, Tong Mei

AU - Jeng, Jiiang Huei

PY - 2012/6

Y1 - 2012/6

N2 - 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 E 2 (PGE 2), prostaglandin F 2α (PGF 2α), 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. PGE 2 and PGF 2α 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. PGE 2 and PGF 2α may potentially regulate inflammatory processes by the inhibition of VCAM-1.

AB - 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 E 2 (PGE 2), prostaglandin F 2α (PGF 2α), 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. PGE 2 and PGF 2α 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. PGE 2 and PGF 2α may potentially regulate inflammatory processes by the inhibition of VCAM-1.

KW - Dental pulp cells

KW - inflammation

KW - interleukin-1β

KW - prostanoids

KW - vascular cell adhesion molecule

UR - http://www.scopus.com/inward/record.url?scp=84861202805&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84861202805&partnerID=8YFLogxK

U2 - 10.1016/j.joen.2012.02.030

DO - 10.1016/j.joen.2012.02.030

M3 - Article

VL - 38

SP - 774

EP - 779

JO - Journal of Endodontics

JF - Journal of Endodontics

SN - 0099-2399

IS - 6

ER -