Glucose transporter 4 mediates LPS-induced IL-6 production in osteoblasts under high glucose conditions.


Journal

Journal of oral science
ISSN: 1880-4926
Titre abrégé: J Oral Sci
Pays: Japan
ID NLM: 9808942

Informations de publication

Date de publication:
26 Sep 2020
Historique:
pubmed: 31 8 2020
medline: 30 9 2020
entrez: 1 9 2020
Statut: ppublish

Résumé

Diabetes causes hyperglycemic disorders due to insufficient activity of insulin, and it also increases blood glucose level. Recent studies have reported the relationship between diabetes and periodontal disease. Periodontitis is advanced by inflammatory cytokines stimulated with LPS. The purpose of this study was to investigate the effects of hyperglycemia on the expression of inflammatory cytokines induced by LPS in osteoblasts. Cells were cultured for 7 and 14 days in the presence or absence of LPS and glucose. The expression mRNA level of IL-6, RANKL and OCN was determined using real-time PCR. The protein expression of IL-6 and RANKL was also measured using ELISA. LPS and glucose increased the mRNA expression of IL-6, coupled with a decrease in the mRNA expression of OCN, which is associated with IL-6 and glucose. It also increased the protein expression of IL-6 compared to LPS. However, LPS+Glucose did not affect the mRNA and protein expression of RANKL. Furthermore, GLUT4 inhibitor, WZB117, blocked the stimulatory effect of glucose on LPS-induced IL-6 mRNA expression. WZB117 did not affect LPS-reduced OCN mRNA expression. These results suggest that high glucose levels increase LPS-induced IL-6 expression mediated by GLUT4.

Identifiants

pubmed: 32863319
doi: 10.2334/josnusd.20-0010
doi:

Substances chimiques

Glucose Transport Proteins, Facilitative 0
Glucose Transporter Type 4 0
Interleukin-6 0
Lipopolysaccharides 0
SLC2A4 protein, human 0
Glucose IY9XDZ35W2

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

423-426

Auteurs

Shunichiro Kato (S)

Division of Applied Oral Sciences, Nihon University Graduate School of Dentistry.

Natsuko Tanabe (N)

Department of Biochemistry, Nihon University School of Dentistry.
Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry.

Mayu Nagao (M)

Department of Physiology and Pharmacology, Schulich School of Medicine & Dentistry, and Bone and Joint Institute, Western University.

Jumpei Sekino (J)

Department of Dysphagia Rehabilitation, Nihon University School of Dentistry.

Keiko Tomita (K)

Division of Applied Oral Sciences, Nihon University Graduate School of Dentistry.

Mayu Sakai (M)

Division of Applied Oral Sciences, Nihon University Graduate School of Dentistry.

Kimiko Abe (K)

Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry.
Department of Dysphagia Rehabilitation, Nihon University School of Dentistry.

Naoto Suzuki (N)

Department of Biochemistry, Nihon University School of Dentistry.
Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry.

Koichiro Ueda (K)

Division of Functional Morphology, Dental Research Center, Nihon University School of Dentistry.
Department of Dysphagia Rehabilitation, Nihon University School of Dentistry.

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Classifications MeSH