These findings suggest that the vitamin D pathway exists in hGFs and hPDLCs and plays an important role in immune defense in periodontal soft tissues.
Background The purpose of present study was to explore the mechanism of nuclear factor-kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/protein kinase B(PKB/Akt) and mitogen-activated protein kinase (MAPK) signaling pathways after intervention of advanced glycosylation end products (AGEs) on rat bone-marrow stromal cells (BMSCs). Methods Prepare and identify AGEs. BMSCs were isolated from 16 SD rats and cultured with different concentration of AGEs. Cell viability was detected by cell counting kit-8 (CCK-8). BMSCs were cultured with AGEs (0.25 mg/ml) for 30 min, 12 h, 24 h, 72 h and 120 h. In addition, BMSCs were cultured with AGEs, AGEs + JNK inhibitor and AGEs + P38 inhibitor for 24 h and 48 h, respectively. Western blotting and RT-PCR were used to determine the protein and mRNA expression levels, respectively. Results Cell viability of BMSCs was significantly correlated with concentration and effect time of AGEs (P < 0.05), and the most appropriate concentration was 0.25 mg/ml. AGEs stimulation significantly increased the protein expression levels of NF-κB p65, JNK, p38 (P < 0.05), decreased IκB (P < 0.05), but had no effect on the protein expression of Akt in BMSCs (P > 0.05). At the mRNA level, JNK and p38 inhibitors significantly reduced the levels of NF-κB p65, p38 and JNK, increased IκB (P > 0.05), but had no effect on Akt in BMSCs (P > 0.05). At the protein level, JNK and p38 inhibitors notably decreased the expression of NF-κB p65, p38, p-JNK, P-IκB and JNK (P < 0.001), and increased IκB (P < 0.05). Conclusion Advanced glycosylation end products can inhibit the proliferation of bone-marrow stromal cells through activating MAPK pathway.
Background: Over the last decade, there has been an increasing number of clinical and laboratory evidence supporting associations between Polycystic ovary syndrome (PCOS) and periodontitis, but few studies have been conducted on the underlying mechanisms of the two diseases through the transcriptomic approach. In this study, gene co-expression networks between PCOS and periodontitis were analyzed by bioinformatics tools. Methods: PCOS and periodontitis expression data were downloaded from the GEO database, and the differentially expressed genes (DEGs) were identified. After obtaining Intersected genes, GO and KEGG pathway enrichment analysis and random forest (RF) algorithm were used to screen hub genes in PCOS and periodontitis. The functions of the hub genes were analyzed by GSEA, and the correlations between hub genes and immune infiltration in two diseases were examined. Furthermore, a TF-ceRNA regulatory network of hub genes was constructed. Results: There were 1,661 DEGs in PCOS and 701 DEGs in periodontitis compared to the controls. After overlapping, 66 intersected genes were shown to be involved in PCOS and periodontitis, and were mainly enriched in immune and inflammation-related biological processes and pathways. 40 common genes were selected from the PPI network constructed by STRING. The RF algorithm demonstrated that ACSL5, NLRP12, CCRL2, and CEACAM3 were hub genes in PCOS and periodontitis, and the GSEA result revealed their close relationship with the antigen processing and presentation, and chemokine signaling pathway. Moreover, the data showed that those 4 hub genes may serve as diagnostic genes for PCOS and periodontitis. Conclusion: This study identified ACSL5, NLRP12, CCRL2, and CEACAM3 as the diagnostic genes at the intersection of PCOS and periodontitis, and establish a ceRNA network, which could provide a molecular basis for future experimental studies on the association between PCOS and periodontitis.
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