Inducing cyclooxygenase-2 expression, prostaglandin E2 and prostaglandin F2α production of human dental pulp cells by activation of toll-like receptor-3, mitogen-activated protein kinase kinase/extracellular signal-regulated kinase and p38 signaling
Dental pulp
Infection/inflammation
0301 basic medicine
03 medical and health sciences
Toll-like receptor 3
Prostaglandin
Dentistry
RK1-715
Original Article
Signal transduction
Cyclooxygenase
DOI:
10.1016/j.jds.2023.11.009
Publication Date:
2023-11-25T12:26:28Z
AUTHORS (7)
ABSTRACT
/purpose: Bacterial infection was the major etiology for pulpal/root canal infection. This study aimed to investigate activation of toll-like receptor-3 (TLR) on cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) PGF2α production human dental pulp cells (HDPCs) associated signaling. HDPCs were exposed different concentrations Poly (I:C) (a TLR3 activator). Cell viability determined by 3- (4,5-Dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay alkaline phosphatase (ALP) activity evaluated ALP staining. Activation extracellular signal-regulated kinase (ERK) p38 immunofluorescent The COX-2 protein analyzed Western blot. PGE2 measured enzyme-linked immunosorbent assay. mRNA studied real-time polymerase-chain reaction. Moreover, Poly(I:C) with/without U0126 or SB203580 treatment analysis prostanoid conducted. showed little effect activity, but decreased HDPCs. It stimulated expression. induced activated p-ERK, p-p38 Treatment mitogen-activated (MEK)/ERK inhibitor) attenuated (I:C)-induced as well production. is involved in inflammatory responses tissues, via MEK/ERK, signaling mediate production, contributing pathogenesis progression pulpal/periapical diseases.
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