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HtrA1 may regulate the osteogenic differentiation of human periodontal ligament cells by TGF-β1
| Content Provider | Semantic Scholar |
|---|---|
| Author | Zhang, Qi |
| Copyright Year | 2015 |
| Abstract | AbstractPeriodontal 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-β (TGF-β) 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-β1. Firstly we confirmed the mRNA expression of HtrA1 and TGF-β1 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-β1. In contrast, knockdown of HtrA1 suppressed the osteogenic differentiation with down-regulation of TGF-β1. These findings suggested that HtrA1 plays a positive role in hPDLCs osteogenic differentiation and may regulate this process by TGF-β1. |
| Starting Page | 137 |
| Ending Page | 144 |
| Page Count | 8 |
| File Format | PDF HTM / HTML |
| DOI | 10.1007/s10735-015-9612-9 |
| PubMed reference number | 25726184 |
| Journal | Medline |
| Volume Number | 46 |
| Alternate Webpage(s) | https://ss.bjmu.edu.cn/Sites/Uploaded/File/2016/12/276361844195389385401692497.pdf |
| Alternate Webpage(s) | https://doi.org/10.1007/s10735-015-9612-9 |
| Journal | Journal of Molecular Histology |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |