Shenzhen Key Laboratory for Tissue Engineering

Shenzhen, China

Shenzhen Key Laboratory for Tissue Engineering

Shenzhen, China
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Yang L.,Shenzhen University | Zhu W.,Shenzhen University | Zhu W.,Shenzhen Key Laboratory for Tissue Engineering | Cui J.,Guangzhou University | And 12 more authors.
Journal of Biomaterials and Tissue Engineering | Year: 2016

Objective: Bone marrow mesenchymal stem cells (BMSCs), as seed cells, were infected with lentiviruses carrying hypoxia-inducible factor-1α (HIF-1α and combined with nano-hydroxyapatite (Nano-HA) artificial bone. The composite artificial bone was implanted to the defect site of rabbit radius to investigate the repairing effect of HIF-1α on bone defects. Methods: Recombinant HIF-1α lentiviral plasmids were constructed and transfected into 293Ta cells. Rabbit tibial bone marrow was aspirated to isolate and cultivate BMSCs using adherent culture method. The cultivated cells were identified by morphological observations and flow cytometry. BMSCs were infected with lentiviruses harboring HIF-1α, and co-cultured with Nano-HA to obtain HIF-1α-eGFP/BMSCs/Nano-HA artificial bone. The artificial bone cultured in vitro was implanted to the bone defect site of rabbit radius. Thirty New Zealand white rabbits were used and randomly and equally divided into 3 groups. At week 12 after an operation, the rabbit radius specimens were determined by gross observations, X-rays imaging, and pathological tests to analyze the healing status of the radial bone defects. Results: 1. At 48 h after the transfection of lentiviral plasmids harboring HIF-1α into 293Ta cells. At week 12 after the operation, the specimens of various groups were detected by gross observations, X-ray imaging, and histological method. Results showed that both HIF-1α-eGFP/BMSCs/Nano-HA composite artificial bone in group A and BMSCs/Nano-HA composite artificial bone in group B could promote the bone defect repair. Furthermore, the HIF-1α-eGFP/BMSCs/Nano-HA composite artificial bone in group A formed more new bones, and therefore had a stronger bone-defect repairing ability than group B. In group C, osseous union was not present in the bone defect site, indicating the failure of bone defect repair. Conclusion: BMSCs function as the seed cells of bone tissue engineering to facilitate osteogenesis. HIF-1α genes promote the BMSCs to stimulate osteogenesis and angiogenesis, and increase the formation of new bone tissues, thus leading to more effective bone defect repair. With the good osteoconductivity of Nano-HA, HIF-1α-eGFP/BMSCs/Nano-HA composite artificial bones possess. © 2016 American Scientific Publishers. All rights reserved.


Zhang J.,Guangdong Pharmaceutical University | Zhang J.,Shenzhen Second Peoples Hospital | Zhang J.,Shenzhen Key Laboratory for Tissue Engineering | Wang D.,Shenzhen Second Peoples Hospital | And 7 more authors.
Oncology Letters | Year: 2015

A body of evidence has indicated that microRNAs (miRNAs) may have significant roles in cancer. Aberrant expression of miRNAs has frequently been observed in various human malignancies, including osteosarcoma (OS). However, the roles of miRNAs in OS remain poorly understood. In the present study, high-throughput deep sequencing was performed to screen for deregulated miRNAs in OS. Screening identified 310 miRNAs which were significantly overexpressed and 41 miRNAs which were significantly downregulated (>2-fold) in OS samples, compared with adjacent non-tumor bone tissues. Among these miRNAs, miR-33a-5p was notably downregulated. TaqMan reverse transcription-polymerase chain reaction analysis further verified that miR-33a-5p expression was significantly reduced in a large cohort of human OS samples. Enhancing miR-33a-5p expression via transfection with miR-33a-5p precursor significantly inhibited OS cell growth, suggesting potential antitumor properties of miR-33a-5p. The results of the present study provide novel insights into the miRNAs involved in OS, and suggest that miR-33a-5p may function as a tumor suppressor in OS. Therefore, miR-33a-5p may be able to serve as a diagnostic and therapeutic target for OS treatment. © 2015, Spandidos Publications. All rights reserved.

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