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Lipoxin A4 (LXA4) has been identified as the braking signal of inflammation, but the specific role of LXA4 in regulating the regenerative potential of periodontal ligament stem cells (PDLSCs) remains unclear. The aim of this study was to investigate whether and, if so, how LXA4 improves the osteogenic differentiation of PDLSCs in a lipopolysaccharide (LPS)‐induced inflammatory environment. We detected the effects of LXA4 on the osteogenic differentiation of PDLSCs in vitro and explored the bone regenerative potential of LXA4‐treated inflammatory PDLSCs in vivo using a calvarial critical sized defect model in male rats. RNA sequencing, real‐time PCR and western blot were performed to elucidate the relevant potential mechanisms. Results showed that LXA4 promoted the proliferation, migration and osteogenic differentiation of PDLSCs in vitro, and effectively improved the impaired osteogenic capacity of PDLSCs induced by LPS both in vitro and in vivo. Mechanistically, LXA4 significantly promoted the PI3K/AKT phosphorylation under inflammatory conditions. Additionally, LY294002 (a PI3K inhibitor) blocked the effect of LXA4, suggesting that the PI3K/AKT pathway is a key signaling pathway that mediates the effect of LXA4 on the osteogenesis of inflammatory PDLSCs. These findings indicate LXA4 may be a promising strategy for periodontal regeneration using inflammatory PDLSCs. [ABSTRACT FROM AUTHOR]

Fat transplantation is increasingly used in breast augmentation; and recently, the issue of safety concerns from a cellular and molecular point of view has been raised. In this study, attentions were paid to the interaction between adipose-derived stem cells (ADSC) and mammary epithelial cells: human breast cancer cell line - 100 (HBL - 100) cells were used to simulate the normal microenvironment in breast tissue, ADSCs were harvest from human and co-cultured with HBL-100 cells. It was found that ADSCs formed tube-like structures in the co-culture with HBL-100 cells in contrast to the normal morphology of ADSCs in the control group. In addition, the immunofluorescence imaging showed that cytokeratin 18 and 19 (CK18 and 19) were significantly expressed in ADSCs after the co-culture with HBL-100 cells. The ultrastructure of those ADSCs also showed epithelial changes. In conclusion, ADSCs are not biological stable when co-cultured with HBL-100 cells. They differentiate into epithelial-like cells with the expression of epithelial surface marks (CK 18, 19) and form tube-like structures. This may offer an important evidence for the further study of clinical application of transplanting ADSCs rich adipose tissue into the breast in the future. [ABSTRACT FROM AUTHOR]

Background: Segmental bone defect is still a challenge to orthopedic surgeons. Currently available therapies for segmental bone defects have some drawbacks. Tissue engineering using pluripotent stem cells is a new, promising method for bone repair. The present study aims to promote the effect of bone defect repair using the tissue engineered bone in combination with vascularized periosteal flaps. Methods: The adenoviral vector carrying Cbfa1 transduced rabbit adipose-derived mesenchymal stem cells and gene modified tissue engineering bone (GMB) were constructed. Rabbits with radial defects were implanted with the GMB together with vascularized periosteum (group A); or GMB with free periosteum (group B); or GMB (group C), and scaffold (group D). The bone repair effect was evaluated at 4, 8, or 12 wk, respectively, after the operations. Results: Cbfa1 proteins were strongly expressed in adipose stem cells (ADSCs) that formed a stratified network on the inner surface of the polylactic acid/ polycaprolacton (PLA/PCL) pores. Bone repair was well achieved in the rabbits treated with the Cbfa1-expressing ADSCs and vascularized flap that was markedly better than those treated with either Cbfa1-expressing ADSCs alone or with vascularized flap alone. Conclusions: Combination with implanting the Cbfa1 gene-modified tissue-engineered bone and vascularized periosteum can better repair the segmental bone defects by stimulating osteogenesis, osteoinduction, and osteoconduction than using either one of the approaches. [Copyright &y& Elsevier]