Cellular reprogramming最新文献

Zinc is an essential trace element for bone growth and bone homeostasis in the human body. Bone mesenchymal stem cells (BMSCs) are multipotent progenitors existing in the bone marrow stroma with the capability of differentiating along multiple lineage pathways. Zinc plays a paramount role in BMSCs, which can be spurred differentiating into osteoblasts, chondrocytes, or adipocytes, and modulates the formation and activity of osteoclasts. The expression of related genes also changed during the differentiation of various cell phenotypes. Based on the important role of zinc in BMSC differentiation, using zinc as a therapeutic approach for bone remodeling will be a promising method. This review explores the role of zinc ion in the differentiation of BMSCs into various cell phenotypes and outlines the existing research on their molecular mechanism.

Dental pulp stem cells (DPSCs) from pulpitis patients showed defective osteogenic differentiation. However, as the most well-studied histone acetyltransferase, the impaired general control nonrepressed protein 5 (GCN5) plays essential roles in various developmental processes. The aim of this study was to investigate the effect of GCN5 on DPSCs odontogenic differentiation. The healthy dental pulp tissues were obtained from the extracted impacted third molar of patients with the informed consent. DPSCs were treated with a high concentration of tumor necrosis factor-alpha (TNF-α) (100 ng/mL) and odontogenic differentiation-related gene and GCN5 protein level by Western blot analysis. Proliferation of the DPSCs was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Immunofluorescence staining detected GCN5 and NF-κB signaling for p-p65. The mechanism of GCN5 regulating odontogenic differentiation of DPSCs was determined by small interfering RNA analysis. Our data suggested that TNF-α can significantly reduce mineralization and the expression of dentin matrix acidic phosphoprotein 1 and dentin sialophosphoprotein at higher concentration (100 ng/mL). Meanwhile, it showed that the inflammation in microenvironment resulted in a downregulation of GCN5 expression and GCN5 knockdown caused decreased odontogenic differentiation of DPSCs was also found. In addition, the knockdown of GCN5 increased the expression of phosphorylation of p65, thus activating NF-κB pathway of DPSCs. Meanwhile, NF-κB pathway inhibitor pyrrolidinedithiocarbamic acid reversed the siGCN5 decreased odontogenic differentiation of DPSCs. Altogether, our findings indicated that in inflammatory microenvironments GCN5 plays a protective role in pulpitis impaired odontogenic differentiation of DPSCs by activating NF-κB pathway, which may provide a potential approach to dentin regeneration.

Somatic cell nuclear transfer (SCNT) shows great value in the generation of transgenic animals, protection of endangered animals, and stem cell therapy. The combination of SCNT and gene editing has produced a variety of genetically modified animals for life science and medical research. Rabbits have unique advantages as transgenic bioreactors and human disease models; however, the low SCNT efficiency severely impedes the application of this technology. The difficulty in SCNT may be attributable to the abnormal reprogramming of somatic cells in rabbits. This review focuses on the abnormal reprogramming of cloned mammalian embryos and evaluates the progress and prospects of rabbit somatic cell cloning.