Anti-BMP7 (aa 300-400) polyclonal antibody [HRP]

Objectives: To evaluate a promising 3D scaffold named as FlexBone combined with BMP7 transduced BMSCs in vivo. Methods BMP7 transduced BMSCs were acquired and combined with FlexBone as scaffold. The biocompatibility of FlexBone was evaluated by MTT and duration of BMP7 release was tested using western-blot analysis in vitro. Subsequently, construction of the radial defect model was performed in thirty New Zealand white rabbits. According to types of implant placement, the animals were divided into three groups: FlexBone/BMP7-BMSCs (A); FlexBone/BMSCs (B) and control group (C). The histological staining, radiological examinations, micro-CT scans, and biomechanical tests were used to evaluate effects of the material in process of bone healing at each time point after implant placement. Results: The MTT test showed good proliferation of BMP7-BMSCs on FlexBone over a period of 7 days. The western blot analysis demonstrated that BMP7-BMSCs/FlexBone composites could provide a sustained release of BMP7 for at least 21 days in vitro. The histological staining, X-rays and Micro CT indicated that more newly formed bone tissues were present in group A at 6th and 12th week after implantation, compared with group B postoperatively. Finally, biomechanical tests demonstrated that mechanical properties of the tissue engineered bone in group A were similar to normal bones. Conclusions: The FlexBone exhibited excellent biocompatibility toward BMP7 transduced BMSCs in vitro and could play an effective role in accelerating bone regeneration in vivo.

This study aimed to investigate the role and underlying mechanism of miR-135b in high glucose-induced oxidative stress of renal tubular epithelial cells. Here, in vivo experiments found that compared to the control group, miR-135b expression was significantly up-regulated in the diabetes group, whereas BMP7 mRNA and protein levels were down-regulated. In high glucose-treated renal tubular epithelial cells (HK-2) in vitro, oxidative stress was induced, which up-regulated miR-135b expression. In addition, the regulation of miR-135b on BMP7 expression was confirmed in HK-2 cells. Under high glucose conditions, oxidative stress promoted the apoptosis of HK-2 cells through the up-regulation of miR-135b expression. In vivo experiments indicated that interference with miR-135b improved renal function in mice with diabetic nephropathy. In conclusion, these results indicated that the up-regulation of miR-135b expression induced by oxidative stress promotes the apoptosis of HK-2 cells under high glucose conditions.