Tissue-engineered technology has provided a promising method for the repair of growth plate injuries using biocompatible and biodegradable scaffolds and appropriate cells. The aim of this study was to fabricate oriented ECM scaffolds to imitate the material and structure of a natural growth plate and to investigate whether BMSCs in a scaffold could prevent the formation of bone bridges in an injured growth plate. We developed a natural, acellular and oriented scaffold derived from a growth plate. The oriented scaffold was fabricated using new freeze-drying technology and by cross-linking the microfilaments in the growth plate. From histological examination, the scaffold contained most of the ECM components including GAG and collagen II without cell DNA fragments, and SEM revealed that oriented scaffold had a uniform aperture in the transverse plane and columnar structure in length plane. Cytotoxicity testing with MTT showed no cytotoxic effect of the scaffold extracts on BMSCs. Autogenous BMSCs in oriented scaffolds promoted the regeneration of neogenetic growth plate when repairing an injured growth plate and prevent the formation of bone bridges to reduce the angular deformity and length discrepancy in the proximal tibia in rabbits. The well-characterized ECM-derived oriented growth plate scaffold shows potential for the repair of injured growth plates in young rabbits.

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Osteosarcoma (OS) is the most common bone malignancy in the pediatric population, and it comprises about 3 % of all pediatric tumors. Aberrant expression of the Cullin 4A (CUL4A) is found in many tumor types, but the role of CUL4A in OS progression remains largely unknown. The aim of this study was to investigate the expression and function of CUL4A in OS. CUL4A expression was detected in 30 samples of surgically resected OS and matched tumor-adjacent tissues using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot. Cell proliferation was assessed by MTT, and migration and invasion were analyzed by Transwell and Matrigel assays after CUL4A knockdown in OS in vitro. Our result showed increased CUL4A expression in OS tissues. CUL4A knockdown inhibited the proliferation of MG63 cells. Furthermore, CUL4A siRNA ameliorated the migration and invasion of MG63 cell lines with altered expression of epithelial-mesenchymal transition (EMT)-associated molecules. Taken together, our findings indicate that CUL4A plays a pivotal role in OS progression and may serve as a potential marker for clinical diagnosis and target for therapy.