Fibrous encapsulation that prevents the direct contact between an implant and the bone can cause implant failure.

Objective Autograft microskin transplantation has been widely used as a skin graft therapy in full-thickness skin defect. However, skin grafting failure can lead to a pathological delay wound healing due to a poor vascularization bed. Considering the active role of adipose-derived stem cell (ADSC) in promoting angiogenesis, we intend to investigate the efficacy of autograft microskin combined with ADSC transplantation for facilitating wound healing in a full-thickness skin defect mouse model. Material and methods An in vivo full-thickness skin defect mouse model was used to evaluate the contribution of transplantation microskin and ADSC in wound healing. The angiogenesis was detected by immunohistochemistry staining. In vitro paracrine signaling pathway was evaluated by protein array and Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway, and protein-protein interaction network analysis. Results Co-transplantation of microskin and ADSC potentiated the wound healing with better epithelization, smaller scar thickness, and higher angiogenesis (CD31) in the subcutaneous layer. We found both EGF and VEGF cytokines were secreted by microskin in vitro. Additionally, secretome proteomic analysis in a co-culture system of microskin and ADSC revealed that ADSC could secrete a wide range of important molecules to form a reacting network with microskin, including VEGF, IL-6, EGF, uPAR, MCP-3, G-CSF, and Tie-2, which most likely supported the angiogenesis effect as observed. Conclusion Overall, we concluded that the use of ADSC partially modulates microskin function and enhances wound healing by promoting angiogenesis in a full-thickness skin defect mouse model. Electronic supplementary material The online version of this article (10.1186/s13287-019-1389-4) contains supplementary material, which is available to authorized users.

Osteosarcoma (OS) is the most common primary solid malignant bone tumor, and its metastasis is a prominent cause of high mortality in patients. In this study, a prognosis risk signature was constructed based on metastasis-associated genes. Four microarrays datasets with clinical information were downloaded from Gene Expression Omnibus, and 256 metastasis-associated genes were identified by limma package. Further, a protein-protein interaction network was constructed, and survival analysis was performed using data from the Therapeutically Applicable Research to Generate Effective Treatments data matrix, identifying 19 genes correlated with prognosis. Six genes were selected by the least absolute shrinkage and selection operator regression for multivariate cox analysis. Finally, a three-gene (MYC, CPE, and LY86) risk signature was constructed, and datasets GSE21257 and GSE16091 were used to validate the prediction efficiency of the signature. The survival times of low-and highrisk groups were significantly different in the training set and validation set.Additionally, gene set enrichment analysis revealed that the genes in the signature may affect the cell cycle, gap junctions, and interleukin-6 production. Therefore, the three-gene survival risk signature could potentially predict the prognosis of patients with OS. Further, proteins encoded by CPE and LY86 may provide novel insights into the prediction of OS prognosis and therapeutic targets.differentially expressed genes, metastasis, osteosarcoma, risk signature, survival analysis 1 | INTRODUCTION Osteosarcoma (OS), characterized by malignant mesenchymal cells producing an osteoid matrix and fibrillary stroma, is the most common osseous aggressive cancer in children and juveniles and commonly arises at the terminus of the long bones, including distal femurs, proximal tibias, and proximal humor. 1 According to the National Cancer Institute Surveillance, Epidemiology, and End Results program, the frequency of OS has increased by 0.3% per year over the last decade. 2 With the intensification of chemotherapeutic regimens, the 5-year survival rate of OS patients without metastasis has been improved to 60%-70%. 3 By contrast, the survival rate is only 0%-30% in patients with OS with metastasis, 4 indicating that OS metastasis is associated poor longterm prognosis. However, metastasis-associated molecules Yi Shi and Ronghan He contributed equally to this work.