| Autor: |
Steinecker-Frohnwieser B; Ludwig Boltzmann Institute for Arthritis and Rehabilitation, 5760 Saalfelden, Austria., Lohberger B; Ludwig Boltzmann Institute for Arthritis and Rehabilitation, 5760 Saalfelden, Austria.; Department of Orthopedics and Trauma, Medical University Graz, 8036 Graz, Austria., Eck N; Ludwig Boltzmann Institute for Arthritis and Rehabilitation, 5760 Saalfelden, Austria.; Department of Orthopedics and Trauma, Medical University Graz, 8036 Graz, Austria., Mann A; Division of Special Anaesthesia and Pain Medicine, Medical University of Vienna, 1090 Vienna, Austria., Kratschmann C; Division of Special Anaesthesia and Pain Medicine, Medical University of Vienna, 1090 Vienna, Austria., Leithner A; Department of Orthopedics and Trauma, Medical University Graz, 8036 Graz, Austria., Kullich W; Ludwig Boltzmann Institute for Arthritis and Rehabilitation, 5760 Saalfelden, Austria., Weigl L; Division of Special Anaesthesia and Pain Medicine, Medical University of Vienna, 1090 Vienna, Austria. |
| Abstrakt: |
Nuclear magnetic resonance therapy (NMRT) is discussed as a participant in repair processes regarding cartilage and as an influence in pain signaling. To substantiate the application of NMRT, the underlying mechanisms at the cellular level were studied. In this study microRNA (miR) was extracted from human primary healthy and osteoarthritis (OA) chondrocytes after NMR treatment and was sequenced by the Ion PI Hi-Q™ Sequencing 200 system. In addition, T/C-28a2 chondrocytes grown under hypoxic conditions were studied for IL-1β induced changes in expression on RNA and protein level. HDAC activity an NAD (+) /NADH was measured by luminescence detection. In OA chondrocytes miR-106a, miR-27a, miR-34b, miR-365a and miR-424 were downregulated. This downregulation was reversed by NMRT. miR-365a-5p is known to directly target HDAC and NF-ĸB, and a decrease in HDAC activity by NMRT was detected. NAD + /NADH was reduced by NMR treatment in OA chondrocytes. Under hypoxic conditions NMRT changed the expression profile of HIF1, HIF2, IGF2, MMP3, MMP13, and RUNX1. We conclude that NMRT changes the miR profile and modulates the HDAC and the NAD (+) /NADH signaling in human chondrocytes. These findings underline once more that NMRT counteracts IL-1β induced changes by reducing catabolic effects, thereby decreasing inflammatory mechanisms under OA by changing NF-ĸB signaling. |
