Hypoxia-inducible factor 1α promotes interleukin 1β and tumour necrosis factor α expression in lipopolysaccharide-stimulated human dental pulp cells.

HIF1α NFκB signalling human dental pulp cells lipopolysaccharide pro-inflammatory cytokine

Journal

International endodontic journal
ISSN: 1365-2591
Titre abrégé: Int Endod J
Pays: England
ID NLM: 8004996

Informations de publication

Date de publication:
May 2020
Historique:
received: 07 05 2019
accepted: 31 12 2019
pubmed: 8 1 2020
medline: 15 4 2020
entrez: 8 1 2020
Statut: ppublish

Résumé

To elucidate the role of HIF1α in pro-inflammatory cytokine mRNA expression from lipopolysaccharide (LPS)-stimulated human dental pulp cells (hDPCs). mRNA expression of interleukin (IL) 1β and tumour necrosis factor (TNF) α in LPS-stimulated hDPCs was determined by quantitative RT-PCR. Expression of nuclear factor kappa B (NFκB) p65 and phospho-NFκB p65 was analysed by Western blotting. Activation of NFκB signalling was measured by luciferase assay using a reporter vector containing an NFκB response element. Enforced expression of HIF1α was induced by transfection of expression vectors with native or constitutively active forms of HIF1α. Expression of HIF1α protein in hDPCs was evaluated by immunocytochemistry and Western blotting. One-way analysis of variance and the Tukey-Kramer test were performed to determine a significant difference (P < 0.05). mRNA expression of IL1β and TNFα, protein expression of phospho-NFκB p65 and LPS-induced NFκB signalling activity were promoted in low oxygen conditions (1% O HIF1α promoted mRNA expression of IL1β and TNFα via NFκB signalling in LPS-stimulated hDPCs, suggesting that HIF1α is involved in the progress of inflammation in dental pulp.

Identifiants

pubmed: 31910287
doi: 10.1111/iej.13264
doi:

Substances chimiques

Interleukin-1beta 0
Lipopolysaccharides 0
NF-kappa B 0
Tumor Necrosis Factor-alpha 0

Types de publication

Journal Article

Langues

eng

Pagination

636-646

Subventions

Organisme : Japan Society for the Promotion of Science
ID : 17H04380

Informations de copyright

© 2020 International Endodontic Society. Published by John Wiley & Sons Ltd.

Références

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Auteurs

M Fujii (M)

Division of Oral Health Sciences, Department of Pulp Biology and Endodontics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

N Kawashima (N)

Division of Oral Health Sciences, Department of Pulp Biology and Endodontics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

K Tazawa (K)

Division of Oral Health Sciences, Department of Pulp Biology and Endodontics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

K Hashimoto (K)

Division of Oral Health Sciences, Department of Pulp Biology and Endodontics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

K Nara (K)

Division of Oral Health Sciences, Department of Pulp Biology and Endodontics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

S Noda (S)

Division of Oral Health Sciences, Department of Pulp Biology and Endodontics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

S Nagai (S)

Division of Oral Health Sciences, Department of Molecular Immunology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

T Okiji (T)

Division of Oral Health Sciences, Department of Pulp Biology and Endodontics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

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