LIPUS suppressed LPS-induced IL-1[alpha] through the inhibition of NF-[kappa]B nuclear translocation via AT1-PLC[beta] pathway in MC3T3-E1 cells

• Published in: Journal of cellular physiology Vol. 232; no. 12; p. 3337
• Main Authors: Nagao, Mayu, Tanabe, Natsuko, Manaka, Soichiro, Naito, Masako, Sekino, Jumpei, Takayama, Tadahiro, Kawato, Takayuki, Torigoe, Go, Kato, Shunichiro, Tsukune, Naoya, Maeno, Masao, Suzuki, Naoto, Sato, Shuichi
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc 01.12.2017
• Subjects: Alveolar bone; Angiotensin; Angiotensin II; Biocompatibility; Biomedical materials; Bone diseases; Bone healing; Calvaria; Cytokines; Gene expression; Healing; Interleukin 1; Interleukin 6; Lipopolysaccharides; mRNA; NF-κB protein; Nuclear transport; Orthopedics; Osteoarthritis; Osteoblasts; Periodontal disease; Periodontal diseases; Periodontics; Rodents; Signal transduction; siRNA; Translocation; Tumor necrosis factor; Ultrasound
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.25777

Inflammatory cytokines, interleukin (IL)-1, IL-6, and TNF-[alpha], are involved in inflammatory bone diseases such as rheumatoid osteoarthritis and periodontal disease. Particularly, periodontal disease, which destroys alveolar bone, is stimulated by lipopolysaccharide (LPS). Low-intensity pulsed ultrasound (LIPUS) is used for bone healing in orthopedics and dental treatments. However, the mechanism underlying effects of LIPUS on LPS-induced inflammatory cytokine are not well understood. We therefore aimed to investigate the role of LIPUS on LPS-induced IL-1[alpha] production. Mouse calvaria osteoblast-like cells MC3T3-E1 were incubated in the presence or absence of LPS (Porphyromonas gingivalis), and then stimulated with LIPUS for 30min/day. To investigate the role of LIPUS, we determined the expression of IL-1[alpha] stimulated with LIPUS and treated with an angiotensin II receptor type 1 (AT1) antagonist, Losartan. We also investigate to clarify the pathway of LIPUS, we transfected siRNA silencing AT1 (siAT1) in MC3T3-E1. LIPUS inhibited mRNA and protein expression of LPS-induced IL-1[alpha]. LIPUS also reduced the nuclear translocation of NF-[kappa]B by LPS-induced IL-1[alpha]. Losartan and siAT1 blocked all the stimulatory effects of LIPUS on IL-1[alpha] production and IL-1[alpha]-mediated NF-[kappa]B translocation induced by LPS. Furthermore, PLC[beta] inhibitor U73122 recovered NF-[kappa]B translocation. These results suggest that LIPUS inhibits LPS-induced IL-1[alpha] via AT1-PLC[beta] in osteoblasts. We exhibit that these findings are in part of the signaling pathway of LIPUS on the anti-inflammatory effects of IL-1[alpha] expression.