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Bone morphogenetic protein-7 promotes chondrogenesis in human amniotic epithelial cells

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Abstract

Bone morphogenetic proteins (BMPs) play important roles at multiple stages of chondrogenesis. This study was undertaken to investigate the potential role of bone morphogenetic protein-7 (BMP-7) in the differentiation of chondrocytes using tissue engineering techniques. The impact of BMP-7 on human amniotic epithelial cells (hAECs) was tested. The hAECs were treated either with recombinant human BMP-7 cDNA or with transforming growth factor beta 1 (TGF-β1) as a positive control for three weeks in vitro. Cartilaginous differentiation and proliferation were assayed by quantitative RT-PCR, histology, and in situ hybridization. Our results were such that hAECs treated with either BMP-7 or TGF-β1 expressed cartilage markers (aggrecan, Sox9, CEP-68, and type II and X collagens) within three weeks. Compared with a control vector, BMP-7 induced a decrease in type I collagen expression, while the transcription of the cartilage-specific type II collagen remained stable. In induction experiments, BMP-7 transgenic hAECs exhibited the largest amount of matrix synthesis. In conclusion, these data indicate that BMP-7 plays an important role in inducing the production of cartilage by hAECs in vitro. Cartilage differentiation and matrix maturation can be promoted by BMPs in a cartilage engineering paradigm. These properties make BMPs promising tools in the engineering of cartilaginous joint bio-prostheses and as candidate biological agents or genes for cartilage stabilisation.

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Acknowledgement

The authors wish to thank Michael Gross and Lian Fu Deng for their excellent technical assistance.

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The authors declare that they have no competing interests.

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Correspondence to Guangrong Yu.

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Zhou, J., Yu, G., Cao, C. et al. Bone morphogenetic protein-7 promotes chondrogenesis in human amniotic epithelial cells. International Orthopaedics (SICOT) 35, 941–948 (2011). https://doi.org/10.1007/s00264-010-1116-3

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  • DOI: https://doi.org/10.1007/s00264-010-1116-3

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