Low-intensity pulsed ultrasound promotes bone morphogenic protein 9-induced osteogenesis and suppresses inhibitory effects of inflammatory cytokines on cellular responses via Rho-associated kinase 1 in human periodontal ligament fibroblasts
| Autor: | Joji Kusuyama, Toshiaki Nakamura, Yukari Ebe, Tetsuya Matsuguchi, Tomokazu Ohnishi, Kazuyuki Noguchi, Nahoko Eiraku, Brent G. Albertson |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Lipopolysaccharides Chemokine Periodontal Ligament Interleukin-1beta Bone morphogenetic protein Biochemistry Bone morphogenetic protein 2 Proinflammatory cytokine 03 medical and health sciences 0302 clinical medicine Osteogenesis Growth Differentiation Factor 2 CXCL10 Humans ROCK1 Noggin Molecular Biology Cells Cultured rho-Associated Kinases biology Chemistry Tumor Necrosis Factor-alpha Cell Differentiation Cell Biology Fibroblasts Cell biology CXCL1 030104 developmental biology Ultrasonic Waves 030220 oncology & carcinogenesis biology.protein Cytokines Inflammation Mediators |
| Zdroj: | Journal of cellular biochemistry. 120(9) |
| ISSN: | 1097-4644 |
| Popis: | Periodontal ligament fibroblasts (PDLFs) have osteogenic capacity, producing bone matrix proteins. Application of bone morphogenic proteins (BMPs) to PDLFs is a promising approach for periodontal regeneration. However, in chronic bone metabolic disorders, such as periodontitis, proper control of accompanying inflammation is essential for optimizing the effects of BMPs on PDLFs. We have previously shown that low-intensity pulsed ultrasound (LIPUS), a medical technology that induces mechanical stress using sound waves, significantly promotes osteogenesis in mesenchymal stem cells. Here, we demonstrate that LIPUS promotes the BMP9-induced osteogenic differentiation of PDLFs. In contrast, BMP2-induced osteogenic differentiation was not altered by LIPUS, probably due to the LIPUS-induced secretion of Noggin, a BMP2 antagonist, from PDLFs. To examine if LIPUS affects inflammatory responses of PDLFs to lipopolysaccharide (LPS) derived from Porphyromonas gingivalis (LPS-PG), we also simultaneously treated PDLFs with LIPUS and LPS-PG. Treatment with LIPUS significantly inhibited the phosphorylation of ERKs, TANK-binding kinase 1, and interferon regulatory factor 3 in LPS-PG-stimulated PDLFs, in addition to inhibiting the degradation of IκB. Furthermore, LIPUS treatment reduced messenger RNA (mRNA) expression of interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, IL-8, C-C motif chemokine ligand 2, C-X-C motif chemokine ligand 1 (CXCL1), CXCL10 and receptor activator of nuclear factor kappa-B ligand, and also diminished IL-1s and tumor necrosis factor a (TNFa)-induced inflammatory reactions. Phosphorylation of Rho-associated kinase 1 (ROCK1) was induced by LIPUS, while ROCK1-specific inhibitor prevented the promotive effects of LIPUS on p38 phosphorylation, mRNA expression of CXCL1 and Noggin, and osteogenesis. The suppressive effects of LIPUS on LPS-PG-stimulated inflammatory reactions were also prevented by ROCK1 inhibition. Moreover, LIPUS treatment blocked inhibitory effects of LPS-PG and IL-1s on osteogenesis. These results indicate that LIPUS suppresses inflammatory effects of LPS-PG, IL-1s, and TNFa and also promotes BMP9-induced osteogenesis through ROCK1 in PDLFs. |
| Databáze: | OpenAIRE |
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