Research Paper|Volume 13, Issue 3|pp 3605—3617

Platelet-derived biomaterials-mediated improvement of bone injury through migratory ability of embryonic fibroblasts: in vitro and in vivo evidence

Yen-Ru Chou¹, Wen-Cheng Lo^2,³, Navneet Kumar Dubey^4,⁵, Jui-Hua Lu^4,⁵, Hen-Yu Liu⁵, Ching-Yu Tsai^4,⁵, Yue-Hua Deng^4,⁵, Chi-Ming Wu⁵, Mao-Suan Huang⁶, Win-Ping Deng^4,^5,^7,⁸

¹Graduate Institute of Biomedical Materials and Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, Taipei, Taiwan
²School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
³Department of Neurosurgery, Taipei Medical University Hospital, Taipei, Taiwan
⁴School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan
⁵Stem Cell Research Center, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan
⁶Department of Dentistry, Taipei Medical University-Shuang Ho Hospital, New Taipei, Taiwan
⁷Graduate Institute of Biomedical and Pharmaceutical Science, Fu Jen Catholic University, Taipei, Taiwan
⁸Department of Life Science, Tunghai University, Taichung, Taiwan

Received: June 4, 2020Accepted: August 31, 2020Published: January 10, 2021

https://doi.org/10.18632/aging.202311

Copyright: © 2021 Chou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Bony injuries lead to compromised skeletal functional ability which further increase in aging population due to decreased bone mineral density. Therefore, we aimed to investigate the therapeutic potential of platelet-derived biomaterials (PDB) against bone injury. Specifically, we assessed the impact of PDB on osteo-inductive characteristics and migration of mouse embryonic fibroblasts (MEFs). Osteogenic lineage, matrix mineralization and cell migration were determined by gene markers (RUNX2, OPN and OCN), alizarin Red S staining, and migration markers (FAK, pFAK and Src) and EMT markers, respectively. The therapeutic impact of TGF-β1, a key component of PDB, was confirmed by employing inhibitor of TGF-β receptor I (Ti). Molecular imaging-based in vivo cellular migration in mice was determined by establishing bone injury at right femurs. Results showed that PDB markedly increased expression of osteogenic markers, matrix mineralization, migration and EMT markers, revealing higher osteogenic and migratory potential of PDB-treated MEFs. In vivo cell migration was manifested by expression of migratory factors, SDF-1 and CXCR4. Compared to control, PDB-treated mice exhibited higher bone density and volume. Ti treatment inhibited both migration and osteogenic potential of MEFs, affirming impact of TGF-β1. Collectively, our study clearly indicated PDB-rescued bone injury through enhancing migratory potential of MEFs and osteogenesis.