Molecular medicine reports
-
The present study aimed to explore the molecular mechanisms associated with intervertebral disc degeneration (IDD) induced by tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β. The microarray dataset no. GSE42611 was downloaded from the Gene Expression Omnibus database. ⋯ In the PPI network, IL6, COL1A1, NFKB1 and HIF1A were hub genes, and in addition, NFKB1 and HIF1A were TFs. Pathways of apoptosis and extracellular matrix ‑ receptor interaction may have important roles in IDD progression. IL6, COL1A1 and the TFs NFKB1 and HIF1A may be used as biomarkers for IDD diagnosis and treatment.
-
The present study aimed to investigate the molecular mechanisms underlying non‑syndromic cleft lip, with or without cleft palate (NSCL/P), and the association between this disease and cancer. The GSE42589 data set was downloaded from the Gene Expression Omnibus database, and contained seven dental pulp stem cell samples from children with NSCL/P in the exfoliation period, and six controls. Differentially expressed genes (DEGs) were screened using the RankProd method, and their potential functions were revealed by pathway enrichment analysis and construction of a pathway interaction network. ⋯ In conclusion, the DEGs for NSCL/P were implicated predominantly in the TGF‑β signaling pathway, the cell cycle and in viral carcinogenesis. The TP53, CDK1, SMAD3, PIK3R1 and CASP3 genes were found to be associated, not only with NSCL/P, but also with cancer. These results may contribute to a better understanding of the molecular mechanisms of NSCL/P.
-
To investigate the molecular pathogenesis of the canonical Wnt/β-catenin pathway in exercise-induced osteoarthritis (OA), 30 male healthy Sprague Dawley rats were divided into three groups (control, normal exercise‑induced OA and injured exercise‑induced OA groups) in order to establish the exercise‑induced OA rat model. The mRNA and protein expression levels of Runx‑2, BMP‑2, Ctnnb1, Sox‑9, collagen Ⅱ, Mmp‑13, Wnt‑3a and β‑catenin in chondrocytes were detected by reverse transcription‑quantitative polymerase chain reaction, western blotting and immunohistochemical staining. The mRNA levels of Runx‑2, BMP‑2 and Ctnnb1 were upregulated in the normal exercise‑induced OA and injured exercise‑induced OA groups; while Runx‑2 and BMP‑2 were upregulated in the injured exercise‑induced OA group when compared with the normal exercise‑induced OA group. ⋯ Ctnnb1, Wnt‑3a and β‑catenin, which are key genes and proteins in the canonical Wnt/β‑catenin pathway, were abnormally expressed in chondrocytes of the exercise‑induced OA rat model. Ctnnb1, β‑catenin and Wnt‑3a were suggested to participate in the pathogenesis of exercise‑induced OA by abnormally activating the Wnt/β‑catenin pathway during physical exercise due to excessive pressure. The results of the present study may provide an improved understanding of the pathogenesis of exercise-induced OA.