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Molecular Mechanisms of Bone Injury and Bone Tissue Regeneration

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Materials Science".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 1063

Special Issue Editor


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Guest Editor
Department of Health Technology, Technical University of Denmark, 2800 Lyngby, Denmark
Interests: regenerative medicine; bone regeneration; degradable medical implants; mechanically competent materials

Special Issue Information

Dear Colleagues,

Bone injury and bone tissue regeneration are regulated by a wide variety of signaling pathways and intracellular networks that are responsible for coordinating the cellular processes of bone formation. Although recent years have seen extensive research on the importance of bone regeneration, the exact mechanism involved in bone formation at different stages of differentiation is still not well understood. The intersection of biomolecular science and materials engineering, emphasizing the development and application of mechanically competent materials, is of significant interest in bone regeneration. Thus, the exploration of the molecular underpinnings and innovations in material science, particularly those integrating clinical and model studies with biomolecular experiments, can reveal the molecular mechanisms of bone formation.

This Special Issue focuses on the recent studies that aim to explore the molecular mechanism and innovations in material science for bone tissue regeneration. Specifically, pure clinical studies are not suitable for this journal; however, submissions that combine clinical insights with molecular-level research are highly encouraged. Studies providing such information are welcomed and will help to elucidate the molecular mechanism of bone injury and bone tissue regeneration.

Dr. Nasim Golafshan
Guest Editor

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Keywords

  • bone formation
  • osteoblast diffrentiation
  • cell-based materials

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Published Papers (1 paper)

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Research

20 pages, 7854 KiB  
Article
Shear Stress Regulates Osteogenic Differentiation of Human Dental Pulp Stem Cells via the p38 Pathway
by Hnin Yu Lwin, Watcharaphol Tiskratok, Maythwe Kyawsoewin, Jeeranan Manokawinchoke, Chutimon Termkwanchareon, Nuttapol Limjeerajarus, Chalida Nakalekha Limjeerajarus, Hiroshi Egusa, Thanaphum Osathanon and Phoonsuk Limraksasin
Int. J. Mol. Sci. 2025, 26(12), 5667; https://doi.org/10.3390/ijms26125667 - 13 Jun 2025
Viewed by 639
Abstract
This study aimed to investigate the effects of shear stress on osteogenic differentiation of human dental pulp stem cells (hDPSCs). The hDPSCs were subjected to shear stress for 24 h before osteogenic induction for 21 days. The mRNA expression of osteogenic markers such [...] Read more.
This study aimed to investigate the effects of shear stress on osteogenic differentiation of human dental pulp stem cells (hDPSCs). The hDPSCs were subjected to shear stress for 24 h before osteogenic induction for 21 days. The mRNA expression of osteogenic markers such as RUNX2, OSX, ALP, COL1A1, OCN, and OPN was evaluated by real-time RT-PCR. Alkaline Phosphatase (ALP) activity and Alizarin Red S (ARS) staining were investigated to confirm osteogenic differentiation and mineralization of hDPSCs, respectively. The protein expression of osterix was shown by immunofluorescence staining and Western blotting. RNA sequencing was performed to investigate how shear stress affects the osteogenic differentiation of hDPSCs, which was validated through p38 inhibitor (SB203580) treatment. Real-time RT-PCR revealed that shear stress enhanced osteogenic marker-gene expression. The increased osterix protein expression was detected on Day 14 in the shear-stress loading group compared to the static group. Shear stress enhanced ALP activity and mineralization, observed on Days 14 and 21. A volcano plot exhibited up- and downregulated genes, while the p38 inhibitor markedly inhibited osteogenic differentiation of hDPSCs triggered by shear stress. In conclusion, shear stress promotes the osteogenic differentiation of hDPSCs through the p38 mitogen-activated protein kinase signaling pathway. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Bone Injury and Bone Tissue Regeneration)
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