Establishment of periodontal tissue regeneration method by using of novel PDLSC cell surface marker and PDL marker

我们发现Semaphorin 3A （Sema3A）可以诱导人牙周韧带（PDL）细胞具有间充质干细胞样特性，Wnt5a可以诱导人牙周韧带细胞（HPDLC）形成胶原纤维，胶原纤维是PDL组织的主要成分。过表达sema3a的HPDLC表现出向功能性成骨细胞和脂肪细胞分化的能力增强，并上调干细胞标记物的表达。同时，Wnt5a抑制HPDLC成骨细胞分化，同时显著增强HPDLC的增殖和迁移，促进HPDLC中pdl相关基因的表达和胶原蛋白的生成。敲低骨膜蛋白基因表达和抑制tgf - β 1功能均可抑制wnt5a诱导的pdl相关基因表达和胶原生成。虽然需要进一步的研究来阐明这两个因子的确切功能机制，但Sema3A和Wnt5a可能是有效再生PDL组织的潜在因子。

We found that Semaphorin 3A (Sema3A) can induce mesenchymal-stem-like properies in human periodontal ligament (PDL) cells, and Wnt5a can induce collagen fibrillogenesis which is main component of PDL tissue, by human PDL cells (HPDLC). Sema3A-overexpressing HPDLC exhibited an enhanced capacity to differentiate into both functional osteoblasts and adipocytes, and upregulated the expression of stem cell markers. Meanwhile, Wnt5a suppressed osteoblastic differentiation of HPDLC, while it significantly enhanced proliferation and migration of HPDLC, and PDL-related gene expression and collagen production in HPDLC. Both knockdown of periostin gene expression and inhibition of TGF-beta1 function suppressed the Wnt5a-induced PDL-related gene expression and collagen production. Although further studies are required to clarify the precise functional mechanism of both factors, Sema3A and Wnt5a can be factors with potential to regenerate PDL tissue efficiently.