TY - JOUR
T1 - Platelet-derived biomaterials-mediated improvement of bone injury through migratory ability of embryonic fibroblasts
T2 - In vitro and in vivo evidence
AU - Chou, Yen Ru
AU - Lo, Wen Cheng
AU - Dubey, Navneet Kumar
AU - Lu, Jui Hua
AU - Liu, Hen Yu
AU - Tsai, Ching Yu
AU - Deng, Yue Hua
AU - Wu, Chi Ming
AU - Huang, Mao Suan
AU - Deng, Win Ping
N1 - Funding Information:
This research was funded by the following grants and agencies: Ministry of Science and Technology Taiwan (MOST 108-2221-E-038-014), Taipei Medical University (TMU 108-5601-004-111) and Stem Cell Research Center, College of Oral Medicine, Taipei Medical University, Taiwan.
Publisher Copyright:
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.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2021/2/15
Y1 - 2021/2/15
N2 - 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.
AB - 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.
KW - bone injury
KW - fibroblasts migration
KW - osteogenesis
KW - platelet-derived biomaterials
KW - TGF-β1
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U2 - 10.18632/aging.202311
DO - 10.18632/aging.202311
M3 - Article
C2 - 33461165
AN - SCOPUS:85101075234
SN - 1945-4589
VL - 13
SP - 3605
EP - 3617
JO - Aging
JF - Aging
IS - 3
ER -