The aim of this study was to evaluate the influence of nanostructures on the surface of titanium, titanium nanosheets (TNS), on the initial attachment, proliferation, and gene expression of various functional factors by rat aortic endothelial cells (RAEC) involved in wound healing. We found that the initial attachment and proliferation of RAECs after 15, 30, 45, 60, and 120 min of culture were increased on titanium surfaces modified with TNS. We also found that the expression of intercellular adhesion molecule 1, von Willebrand, and thrombomodulin transcription factors were elevated in samples containing a TNS-modified disk in compared with unmodified titanium disks during the early stages of wound healing. Our results suggest that nanostructures on titanium surfaces stimulate RAECs to upregulate expression of angiogenic factors and adhesion molecule genes, which play an essential role in controlling inflammation and revascularization during wound healing after implantation.
Vital pulp therapy is the method for the treatment of reversible pulpitis. The ultimate goal of vital pulp therapy is to rapidly regenerate dentin of excellent quality by using an external agent that possesses novel properties such as biocompatibility and bioactivity.Dentin phosphophoryn (DPP) is the most abundant of the non-collagenous polyanionic phospho proteins in dentin. The purpose of this study was to examine the effects of DPP on differentiation and mineralization of odontoblasts. MDPC-23, a rat odontoblast-like cell line was used in this study in vitro and to investigate mineralized-matrix induction ability of DPP in vivo. The cells were cultured with DPP at different concentrations (0, 0.1, 1, and 10 µg/mL). The cell-morphology and proliferation were evaluated. Furthermore, cells were analyzed for mRNA expression of dentin/bone-related proteins by RT-PCR. Moreover, ALPase activity and Alizarin red staining were performed for confirmation of mineralization induced by DPP. The addition of DPP did not affect on proliferation or morphology of MDPC-23. The mRNA expressions of DMP-1 and ALPase were promoted by 0.1, 1 and 10 µg/mL of DPP. Moreover, the mRNA expressions of Osteorix, BSP and OCN were promoted by 1 and 10 µg/mL of DPP but Runx2 and OPN expressions were prominent in case of 10 µg/mL of DPP. The high ALPase activity in MDPC-23 was induced by 1 and 10 µg/mL of DPP. The number of mineralized nodules was higher by addition of 1 and 10 µg/mL of DPP at 7 days. Mineralized-matrix induction was observed after 14 days of implantation of DPP-collagen and RPCs composites on the dorsal side of rat in vivo.This study showed that DPP promotes the differentiation and mineralization of odontoblasts in vitro and induction of mineralization in vivo. Therefore DPP can be a promising candidate for formulating a new pulp capping material.
Natural killer (NK) cells play a key role in inflammation and tumor regression through their ability to migrate into tissues. CXCL8 is one of the chemokines that promote leukocytes invasion and migration into tissues, while the exact molecular mechanisms are not clear at present. In this study, we showed that CXCL8 significantly enhanced CD16+CD56+ human peripheral NK cells degradation of type I collagen. MMP-1 associated with CXCL8-stimulated NK cell surface were co-localized with α2 integrin. The association of pro-MMP-1 with cell surface required a stimulation of CXCL8 in CD16+CD56+ human peripheral NK cells. Anti-MMP-1 antibody inhibited the degradation of type I collagen enhanced by CXCL8. Our data suggested that membrane associated MMP-1 plays a key role in the degradation of matrix proteins in CXCL8 activated CD16+CD56+ human peripheral NK cells. These results suggest that the selective regulations of production and/or localization of MMP-1 in NK cells may lead to effective strategies to control inflammation and tumor elimination.
Tissue regeneration is an important issue in the field of operative dentistry. In a series of previous studies, we demonstrated that tumor necrosis factor (TNF)-α activates the potential for totipotency in human mesenchymal stem cells (hMSCs) and leads to the regeneration of target cells or tissues in the presence of appropriate environmental factors. We proposed that TNF-α is an essential activator of totipotency for hMSCs to differentiate into various types of cells. In this study, we focused on epigenetic control that is closely associated with initialization of cells and examined the expression levels of Oct4, which is a marker of initialization of epigenetic control using the transcription factor set of TNF-α and Activin A. Our results indicate that this transcription factor set induces initialization of hMSCs to ES cells.
Bone remodeling is required for orthodontic tooth movement, and it is essential to clarify the mechanisms. In bone remodeling mechanism, the differentiation into osteoclasts is an important role. It is known that Focal adhesion kinase (FAK) is activated by chemokines, cytokines and engagement with β-1 integrin. Fibronectin is decreased in chronically inflamed connective tissue, such as periodontitis. Focal adhesion kinase (FAK) is a 125-kDa non-receptor type tyrosine kinase that localizes to focal adhesions. FAK is involved in osteoclast bone resorption. Fibronectin is bound to α4 β1-integrin and α5 β1-integrin.In our present study we focused on fibronectin / integrin-mediated the differentiation into osteoclasts and found that this type of the differentiation was mediated through FAK. RANKL stimulation did not enhance the expression of α4, α5 and β1-integrin. Fibronectin inhibited RANKL-induced osteoclasts differentiation in RAW264.7 cells. Fibronectin induced the phosphorylation of FAK. These findings establish fibronectin regulate the differentiation into osteoclasts in bone.