Effects of chronic sleep deprivation on the extracellular signal-regulated kinase pathway in the temporomandibular joint of rats

• Published in: PloS one 2014, Vol.9 (9), p.e107544
• Main Authors: Ma, Chuan, Wu, Gaoyi, Wang, Zhaoling, Wang, Peihuan, Wu, Longmei, Zhu, Guoxiong, Zhao, Huaqiang
• Format: Article
• Language: English
• Subjects: Activation; Adrenocorticotropic hormone; Adrenocorticotropic Hormone - blood; Animals; Arthritis; Biology and Life Sciences; Butadienes - pharmacology; Cartilage, Articular - metabolism; Collagenase 3; Corticosterone; Corticosterone - blood; Destruction; Disease Models, Animal; Electron microscopy; Extracellular signal-regulated kinase; Extracellular Signal-Regulated MAP Kinases - metabolism; Gene expression; Gene Expression Regulation - drug effects; Interstitial collagenase; Kinases; Male; MAP Kinase Signaling System; Matrix metalloproteinase; Matrix Metalloproteinase 1 - genetics; Matrix Metalloproteinase 1 - metabolism; Matrix Metalloproteinase 13 - genetics; Matrix Metalloproteinase 13 - metabolism; Matrix Metalloproteinase 3 - genetics; Matrix Metalloproteinase 3 - metabolism; Medicine and Health Sciences; Metabolic pathways; mRNA; Nitriles - pharmacology; Polymerase chain reaction; Rats; Regulatory mechanisms (biology); Research and Analysis Methods; Rodents; Scanning electron microscopy; Serum levels; Sleep; Sleep deprivation; Sleep Deprivation - genetics; Sleep Deprivation - metabolism; Temporomandibular joint; Temporomandibular Joint - metabolism; Temporomandibular Joint - pathology; Temporomandibular Joint - ultrastructure; Ultrastructure; Western blotting
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0107544

To examine the possible involvement and regulatory mechanisms of extracellular signal-regulated kinase (ERK) pathway in the temporomandibular joint (TMJ) of rats subjected to chronic sleep deprivation (CSD). Rats were subjected to CSD using the modified multiple platform method (MMPM). The serum levels of corticosterone (CORT) and adrenocorticotropic hormone (ACTH) were tested and histomorphology and ultrastructure of the TMJ were observed. The ERK and phospho-ERK (p-ERK) expression levels were detected by Western blot analysis, and the MMP-1, MMP-3, and MMP-13 expression levels were detected by real-time quantitative polymerase chain reaction (PCR) and Western blotting. The elevated serum CORT and ACTH levels confirmed that the rats were under CSD stress. Hematoxylin and eosin (HE) staining and scanning electron microscopy (SEM) showed pathological alterations in the TMJ following CSD; furthermore, the p-ERK was activated and the mRNA and protein expression levels of MMP-1, MMP-3, and MMP-13 were upregulated after CSD. In the rats administered with the selective ERK inhibitor U0126, decreased tissue destruction was observed. Phospho-ERK activation was visibly blocked and the MMP-1, MMP-3, and MMP-13 mRNA and protein levels were lower than the corresponding levels in the CSD without U0126 group. These findings indicate that CSD activates the ERK pathway and upregulates the MMP-1, MMP-3, and MMP-13 mRNA and protein levels in the TMJ of rats. Thus, CSD induces ERK pathway activation and causes pathological alterations in the TMJ. ERK may be associated with TMJ destruction by promoting the expression of MMPs.