Tissue engineering provides a promising way for the regeneration of artificial vertebral laminae. Previous studies have confirmed the feasibility of reconstructing vertebral laminae via hydroxyapatite-collagen I scaffolds and mesenchymal stromal cells. However, there were no studies exploring the degradation of hydroxyapatite-collagen I scaffolds and the function of Wnt/β-catenin pathway in the process. In this study, tissue-engineered laminae (TEL) were constructed by nanohydroxyapatite/collagen I scaffolds and umbilical cord Wharton’s Jelly mesenchymal stromal cells (WJ-MSCs). Cell attachment was observed by scanning electron microscopy, and cell viability was confirmed by Live/Dead staining. The rat models were randomly divided into control and β-catenin inhibition groups. Vertebral lamina defect rat models were made on the fifth lumbar vertebrate, and TEL was implanted into the defect site. After 14 weeks, the newborn laminae were harvested for microcomputed tomography, histology, or transcriptional profile analysis. We found that, for the control group, the newborn lamina formation matched with the scaffold degradation and complete newborn laminae formed at the 14th week; for the β-catenin inhibition group, the scaffold degradation rate overrated the lamina formation and no complete artificial laminae were formed at the 14th week. In addition, the osteoclastic genes, such as Cathepsin K or RANKL, in the control groups were significantly lower than the β-catenin inhibition group, and the antiosteoclastic gene, OPG, in the control group was significantly higher than the β-catenin inhibition group. In conclusion, inhibition of Wnt/β-catenin pathway led to speedy scaffold degradation and deferred artificial lamina formation. Wnt/β-catenin pathway played a critical role in maintaining the balance between scaffold degradation and bone formation in the process of vertebral lamina reconstruction.

中文翻译：

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Wnt/β-Catenin 通路平衡组织工程椎板中的支架降解和骨形成

组织工程为人工椎板的再生提供了一种有前途的方法。先前的研究已经证实了通过羟基磷灰石-胶原 I 支架和间充质基质细胞重建椎板的可行性。然而，没有研究探讨羟基磷灰石-胶原I支架的降解以及Wnt/ β -catenin通路在该过程中的作用。在这项研究中，组织工程薄层 (TEL) 由纳米羟基磷灰石/胶原 I 支架和脐带 Wharton's Jelly 间充质基质细胞 (WJ-MSCs) 构建。通过扫描电子显微镜观察细胞附着，并通过活/死染色确认细胞活力。将大鼠模型随机分为对照组和β-连环蛋白抑制组。以第5腰椎椎体制作椎板缺损大鼠模型，将TEL植入缺损部位。14 周后，收集新生叶片用于显微计算机断层扫描、组织学或转录谱分析。我们发现，对于对照组，新生叶片的形成与支架降解相匹配，并在第 14 周形成完整的新生叶片；对于β-连环蛋白抑制组，支架降解率高估了叶片的形成，第14周没有形成完整的人工叶片。此外，对照组的破骨细胞基因，如组织蛋白酶 K 或 RANKL，显着低于ββ -catenin抑制组，对照组的抗破骨细胞基因OPG显着高于β -catenin抑制组。总之，Wnt/ β -catenin 通路的抑制导致支架快速降解和人工椎板形成延迟。Wnt/ β -catenin通路在椎板重建过程中对维持支架降解与骨形成之间的平衡起到了关键作用。