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首页> 外文期刊>Journal of orthopaedic research >Soluble VEGFR1 reverses BMP2 inhibition of intramembranous ossification during healing of cortical bone defects
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Soluble VEGFR1 reverses BMP2 inhibition of intramembranous ossification during healing of cortical bone defects

机译：可溶性VEGFR1在皮质骨缺陷愈合期间逆转BMP2抑制膜质骨化

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BMP2 is widely used for promotion of bone repair and regeneration. However, bone formation induced by BMP2 is quite variable. Bone forming progenitor cells in different locations appear to respond to BMP2 in different ways, and repair outcomes can vary as a consequence of modulating effects by other factors. In this study, we have examined the effects of VEGF on BMP2-induced repair of a cortical bone defect, a 1mm diameter drill hole, in the proximal tibia of mice. Treatment of the defect with either a bolus of PBS or soluble VEGFR1 (sVEGFR1), a decoy receptor for VEGF, had the same effects on bone formation via intramembranous ossification in the defect and cartilage formation and injured periosteum, during the healing process. In contrast, treatment with BMP2 inhibited intramembranous bone formation in the defect while it promoted cartilage and endochondral bone formation in the injured periosteum compared with mice treated with PBS or sVEGFR1. The inhibitory effect of BMP2 on bone formation was unlikely due to increased osteoclast activity and decreased invasion of blood vessels in the defect. Most importantly, co-delivery of BMP2 and sVEGFR1 reversed the inhibition of intramembranous bone formation by BMP2. Furthermore, the decreased accumulation of collagen and production of bone matrix proteins in the defect of groups with BMP2 treatment could also be prevented by co-delivery of BMP2 and sVEGFR1. Our data indicate that introducing a VEGF-binding protein, such as sVEGFR1, to reduce levels of extracellular VEGF, may enhance the effects of BMP2 on intramembranous bone formation. (c) 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1461-1469, 2017.
机译：BMP2广泛用于促进骨骼修复和再生。然而，BMP2诱导的骨形成相当可变。不同位置的骨形成祖细胞似乎以不同的方式响应BMP2，并且修复结果可能因其他因素调节效应而变化。在这项研究中，我们研究了VEGF对小鼠近端胫骨的BMP2诱导的皮质骨缺损修复的BMP2诱导的修复。用PBS或可溶性VEGFR1（SVEGFR1）的缺陷治疗VEGF的诱饵受体的缺陷对愈合过程中的缺陷和软骨形成和受伤的骨膜中的膜质骨化具有相同的对骨形成的效果。相比之下，用BMP2治疗抑制缺陷中的膜质骨形成，而在与用PBS或SVEGFR1处理的小鼠相比，它在受伤的骨膜中促进了受伤的骨膜中的软骨和中间骨形成。由于破骨细胞活性增加和缺陷中血管的血管减少，BMP2对骨形成对骨形成的抑制作用不太可能。最重要的是，BMP2和SVEGR1的共同递送逆转BMP2抑制膜骨形成。此外，还可以通过共递送BMP2和SVEGFR1，防止在具有BMP2处理的基团缺陷中降低胶原蛋白的积累和骨基质蛋白的产生。我们的数据表明，引入VEGF结合蛋白，例如SVEGFR1，以减少细胞外VEGF的水平，可以增强BMP2对膜质骨形成的影响。 （c）2016骨科研究会。由Wiley期刊，Inc.J orthop Res 35：1461-1469,2017出版。

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