Abstract
Previous studies have shown that Low intensity pulsed ultrasound(LIPUS) prevents polyethylene-debris-induced periprosthetic loosening in vivo, but the details of the mechanism by which it does so remain unclear. In this article, we used polyethylene debris induced RAW 264.7 cells as the in vitro model, and tested the effect of LIPUS on this model. Changes in the level of inflammatory cytokines, cell proliferation, and apoptosis were assessed. Gene overexpression and siRNA technique were applied, and the levels of expression of FBXL2, TRAF6, ERK, and related inflammatory cytokines were also measured. Results indicated that FBXL2-mediated TRAF6 ubiquitination and degradation also plays an important role in aseptic periprosthetic loosening process, and LIPUS prevents such loosening by strengthening this pathway.
Highlights
Joint replacement can dramatically reduce joint pain, restore limb function, and increase quality of life
It is reported that FBXL2 binds with c-terminal of Tumor necrosis factor receptor-associated factor (TRAF), mediates its degradation by ubiquitination[8,9,10,11,12], and prevents inflammation in murine lung injury model infected with Pseudomonas aeruginosa PA10313
This study demonstrated that TRAF6 plays an important role in the process of aseptic inflammatory loosening caused by periprosthetic debris, and low-intensity pulsed ultrasound (LIPUS) was found to inhibit such inflammation through increasing the level of FBXL2, and further increasing ubiquitination of TRAF6
Summary
The polyethylene debris group was associated with far less rates of cell migration than the control group (P < 0.05), and LIPUS was found to prevent this difference from emerging (P > 0.05) (Fig. 1B–C). There was far less FBXL2 expression in the polyethylene debris group than in the control group (P < 0.001), and there was more expression of TRAF6 (P < 0001). The polyethylene debris group showed less expression of FBXL2 and more expression of TRAF6, NF-κB, and p-ERK than the control group. LIPUS was found to increase the expression of FBXL2 and decrease the expression of TRAF6, NF-κB, and p-ERK (Fig. 3). This test confirmed that FBXL2 and TRAF6 had interactions in every group (Fig. 4A). When FBXL2 was overexpressed, the levels of TRAF6 and NF-κB were decreased, and LIPUS was found to enhance this effect. Silencing of FBXL2 increased the level of TRAF6 and NF-κB, and silencing of ERK1/2 decreased the level of TRAF6 and NF-κB (Fig. 6)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
