RESUMO
Abnormal pressure is an important factor that contributes to bone adaptation in the temporomandibular joint (TMJ). We determined the effect of the mitogen-activated protein kinases (MAPK) pathway on the pressure-induced synovial metaplasia procedure for the TMJ, both in vitro and in vivo. Synovial fibroblasts (SFs) were exacted from rat TMJs and exposed to different hydrostatic pressures. The protein extracts were analyzed to determine the activation of ERK1/2, JNK, and p38. Surgical anterior disc displacement (ADD) was also performed on Japanese rabbits, and the proteins of TMJ were isolated to analyze pressure-induced MAPK activation after 1, 2, 4, and 8 weeks. The results showed that the activation of ERK1/2 and JNK in SFs significantly changed with increasing hydrostatic pressure, whereas p38 activation did not change. Moreover, p38 was activated in animals 1 week after surgical ADD. The levels of p38 gradually increased after 2 and 4 weeks, and then slightly decreased but remained higher than in the control 8 weeks after surgical ADD. Nevertheless, JNK was rarely activated after the ADD treatment. Our findings suggest the involvement of MAPK activation in the pressure-induced synovial metaplasia procedure with pressure loading in TMJ.
Assuntos
Sistema de Sinalização das MAP Quinases , Transtornos da Articulação Temporomandibular/metabolismo , Articulação Temporomandibular/patologia , Animais , Células Cultivadas , Fibroblastos/metabolismo , Pressão Hidrostática/efeitos adversos , Cápsula Articular/metabolismo , Cápsula Articular/patologia , Metaplasia , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Coelhos , Ratos , Ratos Sprague-Dawley , Articulação Temporomandibular/metabolismo , Transtornos da Articulação Temporomandibular/etiologia , Transtornos da Articulação Temporomandibular/patologia , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismoRESUMO
We examined the relationship between type 2 diabetes and skin wound healing. GSE38396 was downloaded from the Gene Expression Omnibus database and preprocessed using the RMA function of the Affy package. Differentially expressed genes (DEGs) were identified using the limma package, then DAVID was applied to per-form Gene Ontology functional annotation and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. MicroRNAs and their target genes were screened from the miRecords database and subjected to functional analysis. Finally, the STRING online database was applied to identify the protein-protein interaction relationships, and a combined score > 0.5 was considered to indicate an interaction. A total of 421 DEGs (208 upregulated and 213 downregulated genes) were identified in the skin lymphatic endothelial cells of patients with type II diabetes. Twenty-four microRNAs and 34 target genes were screened, including those involved in cell migration, regulation of cell proliferation, cell death, and cell adhesion regulation, among others. Protein-protein interaction network clustering analysis identified a module composed of 25 genes, and INTERPRO protein domain enrichment analysis showed that the protein domain of the clustering module main-ly contained the insulin-like growth factor binding proteins IGFBP3 and CYR61. IGFBP3 and CYR61 may play important roles in skin wound healing in diabetes patients. This information may be useful for developing methods to treat skin refractory wounds in type II diabetes.