Abstract：
OBJECTIVE: Anterior disk displacement (ADD) is a most common subtype of temporomandibular disorders (TMD), which is promoted by chondrocytes apoptosis. However, the signaling pathways that trigger apoptosis are still unknown. The aim of this study was to investigate the expression of endoplasmic reticulum (ER) stress-related proteins in the condylar cartilage of rabbits following ADD.
METHODS: Sixty healthy adult rabbits were randomly assigned to the experimental and sham-operated control groups (n = 12). The experimental rabbits were subjected to surgical ADD in the right temporomandibular joints. The production of ER stress-related proteins C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78), cleaved caspase-3, and caspase-12 in cartilage was evaluated by immunohistochemistry, quantitative real-time PCR, and Western blot analysis.
RESULTS: Our results showed that the expression of CHOP, GRP78, cleaved caspase-3, and caspase-12 increased significantly along with degenerative changes in cartilage after ADD.
CONCLUSIONS: These results indicate that the ER stress pathway is activated in ADD cartilage and might promote the development of TMD.
METHODS: Sixty healthy adult rabbits were randomly assigned to the experimental and sham-operated control groups (n = 12). The experimental rabbits were subjected to surgical ADD in the right temporomandibular joints. The production of ER stress-related proteins C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78), cleaved caspase-3, and caspase-12 in cartilage was evaluated by immunohistochemistry, quantitative real-time PCR, and Western blot analysis.
RESULTS: Our results showed that the expression of CHOP, GRP78, cleaved caspase-3, and caspase-12 increased significantly along with degenerative changes in cartilage after ADD.
CONCLUSIONS: These results indicate that the ER stress pathway is activated in ADD cartilage and might promote the development of TMD.
摘要：
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