Matrix metalloproteinase 2 (MMP2) was previously reported to play important role in the process of stem cell migration and various differentiation behaviors of muscle-derived mesenchymal stem cells (M-MSCs). However, its role and regulatory mechanism in the osteoblast differentiation and calcification of M-MSCs remain unclear. In the current study, we found that MMP2 could facilitate the osteoblast differentiation and calcification of muscle-derived mesenchymal stem cells by up-regulating the expression of some typical osteogenic differentiation phenotype markers, such as runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and osteocalcin (OCN). Besides, we further demonstrated that MMP2 could be directly targeted by miRNA-29b-3p, which was validated by dual luciferase reporter gene and rescue assays. Moreover, increased expression of MMP2 could contribute to forming more calcium nodules representative for osteoblast calcification verified by the alizarin red staining, vice versa. In conclusion, we identified the role of miRNA-29b-3p/MMP2 relationship in regulating osteoblast differentiation and calcification of M-MSCs, which may complement the effect of MMPs family on the osteoblast differentiation to some extent, providing some potential clinical application value in the promotion of bone formation in the future.
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http://dx.doi.org/10.1016/j.tice.2022.101807 | DOI Listing |
Ann Biomed Eng
January 2025
Department of Biomedical Engineering, Yildiz Technical University, Esenler, 34220, Istanbul, Türkiye.
Titanium (Ti)-based materials are favored for hard tissue applications, yet their bioinertness limits their success. This study hypothesizes that functionalizing Ti materials with chitosan nano/microspheres and calcitriol (VD) will enhance their bioactivity by improving cellular activities and mineralization. To test this, chitosan particles were applied uniformly onto Ti surfaces using electrophoretic deposition (EPD) at 20 V for 3 minutes.
View Article and Find Full Text PDFDelayed fracture healing (DFH), a common complication of post-fracture surgery, exhibits an incompletely understood pathogenesis. The present study endeavors to investigate the roles and underlying mechanisms of miR-656-3p and Bone Morphogenetic Protein-2 (BMP-2) in DFH. It was recruited 94 patients with normal fracture healing (NFH) and 88 patients with DFH of the femoral neck.
View Article and Find Full Text PDFJ Orthop Translat
January 2025
Graduate Institute of Biomedical Materials and Tissue Engineering, College of Biomedical Engineering, Taipei Medical University, 6F Biomedical Technology Building, No. 301, Yuantong Rd., Zhonghe Dist., New Taipei City, 23564, Taiwan.
Background And Objective: Osteoarthritis is a widespread and debilitating condition, particularly affecting the medial compartment of knee joint due to varus knee deformities. Medial opening wedge high tibial osteotomy (MOWHTO) has emerged as an effective treatment, but it comes with challenges like fractures, correction loss, and nonunion, leading to unsatisfactory results in up to 26 % of patients. In response, our study explores the potential of a bioabsorbable magnesium-based bulk metallic glass composite (MgZnCa BMGC) enriched with molybdenum particles as an innovative solution for MOWHTO.
View Article and Find Full Text PDFAdv Ther (Weinh)
January 2025
Division of Plastic & Reconstructive Surgery, University of California, Los Angeles David Geffen School of Medicine, Los Angeles, CA, 90095, USA.
Tissue regeneration involves dynamic dialogue between and among different cells and their surrounding matrices. Bone regeneration is specifically governed by reciprocity between osteoblasts and osteoclasts within the bone microenvironment. Osteoclast-directed resorption and osteoblast-directed formation of bone are essential to bone remodeling, and the crosstalk between these cells is vital to curating a sequence of events that culminate in the creation of bone tissue.
View Article and Find Full Text PDFBone Rep
March 2025
Beijing Institute of Dental Research, Beijing Stomatological Hospital, Capital Medical University, Beijing 100050, China.
Background: Gnathodiaphyseal dysplasia (GDD) is a rare autosomal dominant genetic disease characterized by osteosclerosis of the tubular bones and cemento-osseous lesions of the mandibles. () is the pathogenic gene, however, the specific molecular mechanism of GDD remains unclear. Herein, a knockin ( ) mouse model expressing the human mutation p.
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