OBJECTIVE: The expression of tenascin-C in the synovial membrane of the internal derangement (ID) of the temporomandibular joint (TMJ) has been reported. Hypoxia of the synovial membrane in TMJ is considered to be a cause for the pathophysiology of ID. In this study, we clarify the contribution of hypoxia and interleukin-1beta in the expression of tenascin-C in ID of TMJ. MATERIALS AND METHODS: Synovial fibroblasts and disk cells obtained from ID of TMJs were cultured and treated with interleukin-1beta under normoxia and hypoxia. A Western blot analysis and reverse transcription-polymerase chain reaction analysis were used to identify tenascin-C in cultured synovial fibroblasts and disk cells. In addition, the immunohistochemical staining of tenascin-C was carried out for the specimens of ID of TMJs and normal. RESULTS: The combination of hypoxia and interleukin-1beta caused a significant increase in tenascin-C protein and mRNA of synovial fibroblasts. In contrast, the combination caused no increase in tenascin-C in disk cells. However, the immunohistochemical staining demonstrated tenascin-C to be significantly detected in both the synovial tissue and disks in ID of TMJ. CONCLUSIONS: These results indicate that hypoxic conditions with inflammation modulate the tenascin-C expression in synovial fibroblasts, but not in disk cells.
OBJECTIVE: The expression of tenascin-C in the synovial membrane of the internal derangement (ID) of the temporomandibular joint (TMJ) has been reported. Hypoxia of the synovial membrane in TMJ is considered to be a cause for the pathophysiology of ID. In this study, we clarify the contribution of hypoxia and interleukin-1beta in the expression of tenascin-C in ID of TMJ. MATERIALS AND METHODS: Synovial fibroblasts and disk cells obtained from ID of TMJs were cultured and treated with interleukin-1beta under normoxia and hypoxia. A Western blot analysis and reverse transcription-polymerase chain reaction analysis were used to identify tenascin-C in cultured synovial fibroblasts and disk cells. In addition, the immunohistochemical staining of tenascin-C was carried out for the specimens of ID of TMJs and normal. RESULTS: The combination of hypoxia and interleukin-1beta caused a significant increase in tenascin-C protein and mRNA of synovial fibroblasts. In contrast, the combination caused no increase in tenascin-C in disk cells. However, the immunohistochemical staining demonstrated tenascin-C to be significantly detected in both the synovial tissue and disks in ID of TMJ. CONCLUSIONS: These results indicate that hypoxic conditions with inflammation modulate the tenascin-C expression in synovial fibroblasts, but not in disk cells.
Authors: Y Wu; S E Cisewski; M C Coombs; M H Brown; F Wei; X She; M J Kern; Y M Gonzalez; L M Gallo; V Colombo; L R Iwasaki; J C Nickel; H Yao Journal: J Dent Res Date: 2019-05-24 Impact factor: 6.116
Authors: Gregory J Wright; Jonathan Kuo; Changcheng Shi; Thierry R H Bacro; Elizabeth H Slate; Hai Yao Journal: Ann Biomed Eng Date: 2013-06-15 Impact factor: 3.934