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Proanthocyanidins Promote Osteogenic Differentiation of Human Periodontal Ligament Fibroblasts in Inflammatory Environment Via Suppressing NF-κB Signal Pathway. Huang Jiahui,Liu Lianlian,Jin Shanshan,Zhang Yu,Zhang Liguo,Li Shutong,Song Aimei,Yang Pishan Inflammation Proanthocyanidins (PA) have been proven to suppress inflammation and promote osteogenic differentiation. However, whether PA could promote osteogenic differentiation of human periodontal ligament fibroblasts (HPDLFs) in inflammatory environment is unclear. Here, HPDLFs were stimulated by tumor necrosis factor-α (TNF-α), PA, or their combination, and osteogenic differentiation- and mineralization-associated markers were detected by quantitative real-time polymerase chain reaction (qRT-PCR), alizarin red S staining, and alkaline phosphatase (ALP) activity assay. The result showed that PA significantly upregulated expression of osteogenesis-related genes and proteins and ALP activity in HPDLFs compared with the control in non-inflammatory environment. Moreover, PA significantly reversed inhibition of osteogenesis-related gene and protein expression, ALP activity, and mineralization caused by TNF-α. The underlying mechanism was that PA could regulate osteogenesis of HPDLFs via suppressing nuclear factor-kappa beta (NF-κB) signal pathway. These findings suggest that PA may contribute to bone generation in inflammatory microenvironment via suppressing NF-κB signal pathway. Thus, PA may be a potential treatment agent for periodontal bone regeneration. 10.1007/s10753-019-01175-y
Assessing the effect and related mechanism of naringenin on the proliferation, osteogenic differentiation and endothelial differentiation of human periodontal ligament stem cells. Zhang Li,He Haiyan,Zhang Min,Wu Yujie,Xu Xiaomei,Yang Maohua,Mei Li Biochemical and biophysical research communications Naringenin (NAR) is a natural flavonoid which exerts extensive biological activity, including anti-oxidation, anti-inflammation, anti-cancer, immune regulation and so on. However, the effect and mechanism of NAR in the alveolar bone regeneration are still unclear, which limits its clinical use. Hence, we investigated the effects of NAR in the proliferation, osteogenic and endothelial differentiation of human periodontal ligament stem cells (hPDLSCs) and explore the possible mechanism. The results showed that the proper concentrations (100 nM-10 μM) of NAR can promote the proliferation rate, osteogenic and endothelial differentiation of hPDLSCs. And the 1 μM NAR had the best proliferation promoting effect, while the 10 μM NAR had the best ability of promoting osteogenic and endothelial differentiation. NAR also promoted the mRNA expression of SDF-1 in a concentration dependent manner in PDLSCs. After adding the selective CXCR4 antagonist AMD3100, the osteogenic effect of NAR on PDLSCs is slightly enhanced, while the endothelial differentiation effect of NAR on hPDLSCs is attenuated. In summary, these results indicated that NAR promoted the proliferation of hPDLSCs, and promoted endothelial differentiation of hPDLSCs via SDF-1 to activate SDF-1/CXCR4 signaling pathway. However, the mechanism of which SDF-1 related signaling pathway is activated by NAR to enhance the osteogenic differentiation of hPDLSCs still needs to be investigated. 10.1016/j.bbrc.2020.11.081
Asarylaldehyde enhances osteogenic differentiation of human periodontal ligament stem cells through the ERK/p38 MAPK signaling pathway. Hwang Jin Wook,Park Won-Jong,Han Younho Biochemical and biophysical research communications Periodontitis is an inflammatory disease that affects tooth-supporting tissues. Chronic inflammation can progress to periodontitis, which results in loss of alveolar bone. Asarylaldehyde is a potential substance for bone metabolism present in natural compounds. Here, we propose the application of asarylaldehyde in the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) to prevent bone loss. We investigated the effect of asarylaldehyde on hPDLSCs together with bone differentiation media in vitro. The osteogenic differentiation effect was observed after treatment of hPDLSCs with several concentrations of asarylaldehyde. After 21 days, osteogenic cells were identified by mineralization. We also observed that asarylaldehyde increased the mRNA expression of osteoblast-specific markers in hPDLSCs. Interestingly, asarylaldehyde regulated the levels of alkaline phosphatase (ALP) transcriptional activity through the p38/extracellular-signal-regulated kinase (ERK) signaling pathway. Notably, asarylaldehyde induced hPDLSCs to promote osteogenic differentiation. These results suggest that asarylaldehyde plays a key role in the osteogenic differentiation of hPDLSCs. Asarylaldehyde may be a good candidate for the application of natural compounds in future in periodontal regeneration. 10.1016/j.bbrc.2021.01.053
Pivotal Role of Tenascin-W (-N) in Postnatal Incisor Growth and Periodontal Ligament Remodeling. Frontiers in immunology The continuously growing mouse incisor provides a fascinating model for studying stem cell regulation and organ renewal. In the incisor, epithelial and mesenchymal stem cells assure lifelong tooth growth. The epithelial stem cells reside in a niche known as the cervical loop. Mesenchymal stem cells are located in the nearby apical neurovascular bundle and in the neural plexus. So far, little is known about extracellular cues that are controlling incisor stem cell renewal and guidance. The extracellular matrix protein tenascin-W, also known as tenascin-N (TNN), is expressed in the mesenchyme of the pulp and of the periodontal ligament of the incisor, and is closely associated with collagen 3 fibers. Here, we report for the first time the phenotype of tenascin-W/TNN deficient mice, which in a C57BL/6N background exhibit a reduced body weight and lifespan. We found major defects in the alveolar bone and periodontal ligament of the growing rodent incisors, whereas molars were not affected. The alveolar bone around the incisor was replaced by a dense scar-like connective tissue, enriched with newly formed nerve fibers likely leading to periodontal pain, less food intake and reduced body weight. Using soft food to reduce mechanical load on the incisor partially rescued the phenotype. hybridization and Gli1 reporter mouse experiments revealed decreased hedgehog signaling in the incisor mesenchymal stem cell compartment, which coordinates the development of mesenchymal stem cell niche. These results indicate that TNN deficiency in mice affects periodontal remodeling and increases nerve fiber branching. Through periodontal pain the food intake is reduced and the incisor renewal and the neurovascular sonic hedgehog secretion rate are reduced. In conclusion, tenascin-W/TNN seems to have a primary function in rapid periodontal tissue remodeling and a secondary function in mechanosensation. 10.3389/fimmu.2020.608223