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

我们发现Semaphorin 3A(Sema3A)可以诱导人牙周膜(PDL)细胞具有间充质干细胞样特性，Wnt5a可以通过人牙周膜细胞(HPDLC)诱导PDL组织的主要成分胶原纤维形成。Sema3A过表达的HPDLC表现出向功能性成骨细胞和脂肪细胞分化的能力增强，并上调了干细胞标志物的表达。同时，Wnt5a抑制HPDLC的成骨分化，显著促进HPDLC的增殖和迁移，促进PDL相关基因的表达和胶原的产生。抑制Periostin基因表达和抑制转化生长因子-β1功能均可抑制Wnt5a诱导的PDL相关基因表达和胶原合成。虽然这两个因子的确切作用机制还需要进一步的研究，但Sema3A和WNT5a可能是有潜力高效再生PDL组织的因子。

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.