Archives of oral biology · 2018
Insulin-like growth factor-1 engaged in the mandibular condylar cartilage degeneration induced by experimental unilateral anterior crossbite.
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Wang Dongmei, Yang Hongxu, Zhang Mian, Zhang Hongyun, Lu Lei, Zhang Jing, Wan Xianghong, Wang Meiqing
Аннотация
OBJECTIVE: To investigate the changes in insulin-like growth factor-1 (IGF-1) expression levels in the degenerative mandibular condylar cartilage.
DESIGN: Thirty-six rats were divided into the unilateral anterior crossbite and control groups. The expression levels of IGF-1; IGF-1 receptor (IGF-1R); IGF-binding protein-3 and -5 (IGFBP-3 and -5); proliferating cell nuclear antigen (PCNA); aggrecan; type-I, -II, -VI, and -X collagen; tissue inhibitor of metalloproteinases-1 and -3 (TIMP-1 and -3); metalloproteinases of matrix metalloproteinases-3 and-13 (MMP-3 and -13); a disintegrin and metalloproteinase thrombospondin-4 and -5 (ADAMTS-4 and -5); alkaline phosphatase (ALP); β-glucuronidase; and N-acetyl-β-glucosaminidase in the mandibular condylar cartilage were assessed.
RESULTS: The protein expression levels of IGF-1and IGF-1R were increased from week 4 in the unilateral anterior crossbite group. The mRNA expression level of IGFBP-3 and -5 was upregulated from week 4 and week 2, respectively; that of IGFBP-3 was downregulated at week 8; and that of PCNA, type-II collagen, type-X collagen, aggrecan, TIMP-1, and TIMP-3 was downregulated, whereas that of MMP-3, MMP-13, ADAMTS-4, ADAMTS-5, β-glucuronidase, and N-acetyl-β-glucosaminidase were upregulated from week 2. The positive area size of type-I collagen was increased and that of type VI collagen was decreased from week 2. The positive area size of type X collagen was increased at week 2 but decreased at week 8. The percentage of ALP-positive cells was increased from week 4.
CONCLUSIONS: Unilateral anterior crossbite stimulated the multifarious expression of IGF-1 and IGFBP, which may be linked to chondrocyte proliferation and differentiation in the mandibular condylar cartilage that showed progressive degeneration.
DESIGN: Thirty-six rats were divided into the unilateral anterior crossbite and control groups. The expression levels of IGF-1; IGF-1 receptor (IGF-1R); IGF-binding protein-3 and -5 (IGFBP-3 and -5); proliferating cell nuclear antigen (PCNA); aggrecan; type-I, -II, -VI, and -X collagen; tissue inhibitor of metalloproteinases-1 and -3 (TIMP-1 and -3); metalloproteinases of matrix metalloproteinases-3 and-13 (MMP-3 and -13); a disintegrin and metalloproteinase thrombospondin-4 and -5 (ADAMTS-4 and -5); alkaline phosphatase (ALP); β-glucuronidase; and N-acetyl-β-glucosaminidase in the mandibular condylar cartilage were assessed.
RESULTS: The protein expression levels of IGF-1and IGF-1R were increased from week 4 in the unilateral anterior crossbite group. The mRNA expression level of IGFBP-3 and -5 was upregulated from week 4 and week 2, respectively; that of IGFBP-3 was downregulated at week 8; and that of PCNA, type-II collagen, type-X collagen, aggrecan, TIMP-1, and TIMP-3 was downregulated, whereas that of MMP-3, MMP-13, ADAMTS-4, ADAMTS-5, β-glucuronidase, and N-acetyl-β-glucosaminidase were upregulated from week 2. The positive area size of type-I collagen was increased and that of type VI collagen was decreased from week 2. The positive area size of type X collagen was increased at week 2 but decreased at week 8. The percentage of ALP-positive cells was increased from week 4.
CONCLUSIONS: Unilateral anterior crossbite stimulated the multifarious expression of IGF-1 and IGFBP, which may be linked to chondrocyte proliferation and differentiation in the mandibular condylar cartilage that showed progressive degeneration.
Предметные рубрики MeSH
ADAMTS4 ProteinADAMTS5 ProteinAggrecansAlkaline PhosphataseAnimalsCartilage DiseasesCartilage, ArticularChondrocytesCollagenDisease Models, AnimalFemaleGene Expression ProfilingGene Expression Regulation, EnzymologicGlucuronidaseInsulin-Like Growth Factor Binding Protein 3Insulin-Like Growth Factor Binding Protein 5Insulin-Like Growth Factor IMalocclusionMandibular CondyleMatrix Metalloproteinase 13Matrix Metalloproteinase 3Proliferating Cell Nuclear AntigenRatsRats, Sprague-DawleyReceptor, IGF Type 1Temporomandibular Joint DisordersTissue Inhibitor of Metalloproteinase-1Tissue Inhibitor of Metalloproteinase-3Up-Regulation