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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Deng, Mingzhu Gao, Feifei Liu, Tianfeng Zhan, Weiqiang Quan, Juanhua Zhao, Ziquan Wu, Xuyang Zhong, Zhuolan Zheng, Hong Chu, Jiaqi |
| Abstract | Background Bone defects, resulting from substantial bone loss that exceeds the natural self-healing capacity, pose significant challenges to current therapeutic approaches due to various limitations. In the quest for alternative therapeutic strategies, bone tissue engineering has emerged as a promising avenue. Notably, excretory proteins from Toxoplasma gondii (TgEP), recognized for their immunogenicity and broad spectrum of biological activities secreted or excreted during the parasite’s lifecycle, have been identified as potential facilitators of osteogenic differentiation in human bone marrow mesenchymal stem cells (hBMSCs). Building on our previous findings that TgEP can enhance osteogenic differentiation, this study investigated the molecular mechanisms underlying this effect and assessed its therapeutic potential in vivo. Methods We determined the optimum concentration of TgEP through cell cytotoxicity and cell proliferation assays. Subsequently, hBMSCs were treated with the appropriate concentration of TgEP. We assessed osteogenic protein markers, including alkaline phosphatase (ALP), Runx2, and Osx, as well as components of the BMP/Smad signaling pathway using quantitative real-time PCR (qRT-PCR), siRNA interference of hBMSCs, Western blot analysis, and other methods. Furthermore, we created a bone defect model in Sprague-Dawley (SD) male rats and filled the defect areas with the GelMa hydrogel, with or without TgEP. Microcomputed tomography (micro-CT) was employed to analyze the bone parameters of defect sites. H&E, Masson and immunohistochemical staining were used to assess the repair conditions of the defect area. Results Our results indicate that TgEP promotes the expression of key osteogenic markers, including ALP, Runx2, and Osx, as well as the activation of Smad1, BMP2, and phosphorylated Smad1/5—crucial elements of the BMP/Smad signaling pathway. Furthermore, in vivo experiments using a bone defect model in rats demonstrated that TgEP markedly promoted bone defect repair. Conclusion Our results provide compelling evidence that TgEP facilitates hBMSC osteogenic differentiation through the BMP/Smad signaling pathway, highlighting its potential as a therapeutic approach for bone tissue engineering for bone defect healing. |
| Related Links | https://josr-online.biomedcentral.com/counter/pdf/10.1186/s13018-024-04839-0.pdf |
| Ending Page | 16 |
| Page Count | 16 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| DOI | 10.1186/s13018-024-04839-0 |
| Journal | Journal of Orthopaedic Surgery and Research |
| Issue Number | 1 |
| Volume Number | 19 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2024-07-01 |
| Access Restriction | Open |
| Subject Keyword | Orthopedics Surgical Orthopedics Toxoplasma gondii Bone marrow mesenchymal stem cells Excretory proteins Osteogenic differentiation BMP/Smad signaling pathway Bone defect |
| Content Type | Text |
| Resource Type | Article |
| Subject | Surgery Orthopedics and Sports Medicine |
| Journal Impact Factor | 2.8/2023 |
| 5-Year Journal Impact Factor | 3/2023 |
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