No abstract

The uniform design method was used to study the synthesis of high purity mono-alkyl phosphate (MAP) by cyclic polyphosphoric acid. The main factors influencing the content of mono-alkyl phosphate were investigated. The experimental results were analyzed by regression, and the optimum conditions were found to be as follows: mass pentoxide/mass 85 wt% phosphoric acid/mass octanol = 14.2/5.62/48.5, reaction temperature: 115°C, reaction time: 8 h. Under the optimized conditions, a high purity mono-alkyl phosphate with 98.6 wt% MAP yield was obtained.

Objective. This work is aimed at revealing the role and the molecular mechanism of connective tissue growth factor 2 (CTGF) in the osteoblast differentiation of periodontal ligament stem cells (PDLSCs). Methods. The osteogenic differentiation of PDLSCs was induced by osteogenic induction medium (OM), and the expression level of osteogenic related proteins ALP, RUNX2, OCN, and CTGF was estimated using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting analysis. We constructed cell lines with CTGF overexpression or knockdown to verify the role of CTGF in the osteoblast differentiation of PDLSCs. Alkaline phosphatase (ALP) staining was introduced to measure the osteoblasts activity, and alizarin red S (ARS) staining was employed to test matrix mineralization. The interaction between CTGF and bone morphogenetic protein-2 (BMP-2) was determined by endogenous coimmunoprecipitation (Co-IP). Results. The expression level of CTGF was increased during the osteogenic induction of PDLSCs. Additionally, CTGF overexpression effectively maintained the stemness and facilitated the osteoblast differentiation in PDLSCs, and CTGF knockdown exerted opposite effects. Moreover, at molecular mechanism, CTGF increased the activity of BMP-2/Smad signaling pathway. Conclusion. This investigation verified that CTGF promotes the osteoblast differentiation in PDLSCs at least partly by activating BMP-2/Smad cascade signal.

Periodontitis and diabetes are both chronic diseases with a complex bidi- rectional relationship. Diabetes increases the risk of periodontitis by two to three times when compared to people who do not have diabetes. In this study, we used microarray analysis to identify differentially expressed lncRNAs and mRNAs in response to advanced glycosylation end prod- ucts (AGEs) and conventional osteogenic induction, and we identified LINC00673 as the target. LINC00673, a recently discovered lncRNA, has been studied in various cancers. However, the function and regulatory mechanism of LINC00673 in PDLSCs exposed to the AGEs microenvi- ronment have never been fully explored. Following that, we predicted an interaction between LINC00673 and miR188-3p and confirmed the direct binding sites of miR-188-3p on LINC00673. MiR-188-3p overexpres- sion resulted in increased osteogenic differentiation, whereas LINC00673 overexpression reversed its suppression, indicating that LINC00673 acts as a competing endogenous RNA for miR-188-3p. By suppressing one another, LINC00673 and miR-188-3p form a network that controls LEP, its target gene. By inhibiting the canonical Wnt pathway, LEP decreased bone formation in PDLSCs. In conclusion, our findings provide new evi- dence that this lncRNA-miRNA (microRNA) regulatory network plays an important role in the osteogenic differentiation of PDLSCs and has the potential to be a therapeutic target for diabetes-related periodontitis.