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在核脉中诱导血管生成

Sheela R Damle¹, Agata K Krzyzanowska¹, Maximilian K Korsun¹

¹HSS Research Institute, Hospital for Special Surgery, 515 E 71st Street, New York, NY 10021, USA.

|October 27, 2023

概括

用骨形态遗传蛋白 (BMP) 和血管原因子进行的椎间盘间基因治疗可以促进骨的形成. 然而,骨生长仍然在IVD外部,这表明它不适合骨质生成.

科学领域:

脊柱融合研究的研究.
再生医学是一种再生医学.
组织工程是组织工程.

背景情况:

骨形态遗传蛋白 (BMP) 基因传递到椎间盘 (IVD) 通常会诱导盘外的骨形成.
IVD微环境被认为不利于骨质生成和血管化.
需要策略来增强椎间盘内骨的形成和融合.

研究的目的:

调查IVD矩阵降解和增强的血管化是否可以促进椎间盘内骨质生成和脊髓融合.
评估冠状腺酶-ABC (chABC) 和血管内皮生长因子 (VEGF) 对IVD内BMP驱动的骨质生成的影响.

主要方法:

易斯大鼠接受了基因修改细胞 (BMP2/BMP7或VEGF165) 的外科内盘内输送,有或没有chABC.
进行了放射性,组织学和生物力学分析,以评估骨的形成和融合.
西式冲泡被用于分析可溶性Flt1 (sFlt) 水平.

主要成果:

BMP和VEGF/BMP治疗导致硬度增加,骨产生和融合,但骨形成是IVD外部的.
chABC治疗影响了BMP驱动的骨质生成,减少了蛋白质甘氨酸,并促进了IVD血管生成.
通过chABC治疗,可溶性Flt1从IVD矩阵中释放出来,这表明血管生成的机制.

结论:

可以操纵IVD微环境以促进血管入侵.
虽然没有实现盘内骨质生成,但这些发现表明增强脊髓融合疗法的潜在途径.

关键词:

血管新生的产生.融合融合融合融合融合融合融合融合融合基因传递基因传递基因传递椎间盘之间的椎间盘.骨质发生过程 (osteogenesis)蛋白质甘氨酸酶核脉冲性脉冲性脉冲性

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