Feng Ding1, Jing Wang1, Guoxiong Zhu1, Huaqiang Zhao2, Gaoyi Wu1, Lei Chen3. 1. Department of Stomatology Jinan Military General Hospital Jinan 250000, China. 2. School of Stomatology of Shandong University, Shandong Provincial Key Laboratory of Oral Tissue Regeneration Jinan 250012, China. 3. Department of Stomatology Jinan Military General HospitalJinan 250000, China; Department of Orthodontics, Jinan Stomatological HospitalNo. 101, Jing Liu Road, Jinan 250001, China.
Abstract
BACKGROUND: To examine the possible regulatory mechanisms of osteopontin (OPN) and the nuclear factor-κB (NF-κB) signaling pathway in the temporomandibular joint (TMJ) of rats subjected to chronic sleep deprivation (CSD). METHODS: Rats were subjected to CSD using the modified multiple platform method. The histomorphology of the TMJ was observed by hematoxylin-eosin staining. OPN and NF-κB/p65 expression were detected by immunohistochemical and immunofluorescence staining together with western blotting. The condylar chondrocytes were isolated from the rat TMJ and treated with recombinant OPN (r-OPN) before detection for the expression of NF-κB/p65 and matrix metalloproteinases (MMPs). Western blotting and reverse transcription-polymerase chain reaction were performed to determine the expression of MMP-1, MMP-3, MMP-9, and MMP-13 in the TMJ and chondrocytes respectively. RESULTS: There was a statistically significant difference in OPN and NF-κB/p65 expression between the CSD group and control (CON) group. OPN and NF-κB/p65 expression was increased in the CSD group as compared with in the CON group. NF-κB/p65 expression was significantly increased by r-OPN treatment in the chondrocytes. Furthermore, MMP-1, MMP-3, MMP-9, and MMP-13 production was also remarkably elevated in the CSD group as well as in the chondrocytes. Treatment with 1 μg/ml r-OPN for 48 h led to the highest production of inflammatory cytokines in chondrocytes. CONCLUSIONS: CSD causes pathological alterations in the TMJ. OPN treatment activates the NF-κB signaling pathway and stimulates MMPs in the TMJ and condylar chondrocytes through NF-κB signaling pathway. Chondrocytes treated with 1 μg/ml r-OPN for 48 h produced the highest level of inflammatory cytokines.
BACKGROUND: To examine the possible regulatory mechanisms of osteopontin (OPN) and the nuclear factor-κB (NF-κB) signaling pathway in the temporomandibular joint (TMJ) of rats subjected to chronic sleep deprivation (CSD). METHODS:Rats were subjected to CSD using the modified multiple platform method. The histomorphology of the TMJ was observed by hematoxylin-eosin staining. OPN and NF-κB/p65 expression were detected by immunohistochemical and immunofluorescence staining together with western blotting. The condylar chondrocytes were isolated from the rat TMJ and treated with recombinant OPN (r-OPN) before detection for the expression of NF-κB/p65 and matrix metalloproteinases (MMPs). Western blotting and reverse transcription-polymerase chain reaction were performed to determine the expression of MMP-1, MMP-3, MMP-9, and MMP-13 in the TMJ and chondrocytes respectively. RESULTS: There was a statistically significant difference in OPN and NF-κB/p65 expression between the CSD group and control (CON) group. OPN and NF-κB/p65 expression was increased in the CSD group as compared with in the CON group. NF-κB/p65 expression was significantly increased by r-OPN treatment in the chondrocytes. Furthermore, MMP-1, MMP-3, MMP-9, and MMP-13 production was also remarkably elevated in the CSD group as well as in the chondrocytes. Treatment with 1 μg/ml r-OPN for 48 h led to the highest production of inflammatory cytokines in chondrocytes. CONCLUSIONS: CSD causes pathological alterations in the TMJ. OPN treatment activates the NF-κB signaling pathway and stimulates MMPs in the TMJ and condylar chondrocytes through NF-κB signaling pathway. Chondrocytes treated with 1 μg/ml r-OPN for 48 h produced the highest level of inflammatory cytokines.
Authors: Marc Schmitter; Alexandra Kares-Vrincianu; Horst Kares; Justo Lorenzo Bermejo; Hans-Jürgen Schindler Journal: Sleep Med Date: 2015-05-11 Impact factor: 3.492