HtrA1 may regulate the osteogenic differentiation of human periodontal ligament cells by TGF-β1
HtrA1 may regulate the osteogenic differentiation of human periodontal ligament cells by TGF-β1
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DOI：
10.1007/s10735-015-9612-9
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发表时间：
2015-04-01
影响因子：
3.2
通讯作者：
Zhang, Qi
中科院分区：
文献类型：
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作者：
Li, Ran;Zhang, Qi
牙周膜(PDL)中的牙周膜细胞(PDLCs)可以分化为成骨细胞，而生理上的PDL虽然位于两个硬组织中，但仍保持着非矿化的空间。但其确切机制仍不清楚。高温需求蛋白A1(HtrA1)是一种关键的矿化调节因子，可通过转化生长因子-β(TGF-β)信号途径抑制成骨。然而，HtrA1在PDLCs成骨分化中的作用尚不清楚。我们推测HtrA1可能在维持牙周膜细胞矿化平衡中发挥重要作用，并可能通过转化生长因子-β1调节人牙周韧带细胞的成骨分化。首先，我们通过RT-PCR证实htrA1和转化生长因子-β1在人牙周膜细胞中的表达，然后基于量子点的免疫荧光证实它们在细胞质中的共定位，免疫共沉淀进一步证实了它们之间的相互作用。慢病毒介导的HtrA1过表达促进了hPDLCs的成骨分化，并上调了TGF-β1的表达。相反，HtrA1基因的敲除抑制了hPDLCs的成骨分化，下调了TGF-β1的表达。这些结果表明，HtrA1在hPDLCs的成骨分化过程中起着积极的作用，并可能通过转化生长因子-β1调节这一过程。
Periodontal ligament cells (PDLCs) in periodontal ligament (PDL) can differentiate into osteoblasts, while physiologically PDL remains non-mineralized space although located two hard tissues. But the exact mechanism of which is still unclear. High-temperature requirement protein A1 (HtrA1) is a key mineralization regulator and could inhibit the osteogenesis by transforming growth factor-beta (TGF-beta) signaling. However, the role of HtrA1 in PDLCs osteogenic differentiation has yet to be clarified. We assume HtrA1 may play an important role in maintaining the balance of PDL mineralization, and may regulate human periodontal ligament cells (hPDLCs) osteogenic differentiation by TGF-beta 1. Firstly we confirmed the mRNA expression of HtrA1 and TGF-beta 1 in hPDLCs by RT-PCR, then QDs-based immunofluorescence demonstrated the co-localization of them in the cytoplasm, and co-immunoprecipitation further confirmed the interaction between them. Lentivirus-mediated HtrA1 overexpression enhanced the osteogenic differentiation of hPDLCs, as well as up-regulation of TGF-beta 1. In contrast, knockdown of HtrA1 suppressed the osteogenic differentiation with down-regulation of TGF-beta 1. These findings suggested that HtrA1 plays a positive role in hPDLCs osteogenic differentiation and may regulate this process by TGF-beta 1.