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      Specific microRNAs are associated with fracture healing phases, patient age and multi-trauma

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          Abstract

          Background

          Immediately after a fracture occurs, a fracture hematoma (fxH) is formed. This fxH plays an important role in fracture healing and, under normal circumstances, aids in generating an environment in which a wide variety of cells orchestrate processes involved in fracture healing. MicroRNAs (miRNAs) may influence these processes. The aim of this study was therefore to determine the miRNA expression signature of human fxH in normal fracture healing and examine the potential influence of clinical parameters on these expression levels.

          Methods

          fxH was harvested from 61 patients (mean age 52 ± 19; 32♀ ) during fracture surgery. miRNAs were isolated, transcribed and pooled for qPCR array analysis and validation. Qiagen fibrosis- and inflammation qPCR arrays were used based on an extensive literature study related to fracture healing and osteogenesis. Additionally, miRNA targets were determined.

          Results

          From the array data, a selection of the twenty most regulated miRNAs, 10 up- and 10 down regulated, was validated in the study population. The expression levels of seven out of these twenty miRNAs were correlated to several clinical parameters. The time interval between trauma and surgery showed to influence the expression of three miRNAs, three other miRNAs were expressed in a patient age dependent manner and one miRNA was associated with the severity of trauma.

          Conclusion

          This study portrayed the role and importance of miRNAs in human fxH, linked to key processes in fracture healing. Seven miRNAs showed to be involved in multiple processes that are important in the fracture healing cascade, such as angiogenesis, mineralisation and cellular differentiation. In silico target analysis revealed 260 mRNA targets for 14 out of the 20 validated miRNAs.

          The Translational Potential of this Article

          These data broaden our view on the potential diagnostic and therapeutic implications of miRNAs in fracture healing.

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          Most cited references39

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          Overview of MicroRNA Biogenesis, Mechanisms of Actions, and Circulation

          Jacob O'Brien, Heyam Hayder, Yara Zayed … (2018)
          MicroRNAs (miRNAs) are a class of non-coding RNAs that play important roles in regulating gene expression. The majority of miRNAs are transcribed from DNA sequences into primary miRNAs and processed into precursor miRNAs, and finally mature miRNAs. In most cases, miRNAs interact with the 3′ untranslated region (3′ UTR) of target mRNAs to induce mRNA degradation and translational repression. However, interaction of miRNAs with other regions, including the 5′ UTR, coding sequence, and gene promoters, have also been reported. Under certain conditions, miRNAs can also activate translation or regulate transcription. The interaction of miRNAs with their target genes is dynamic and dependent on many factors, such as subcellular location of miRNAs, the abundancy of miRNAs and target mRNAs, and the affinity of miRNA-mRNA interactions. miRNAs can be secreted into extracellular fluids and transported to target cells via vesicles, such as exosomes, or by binding to proteins, including Argonautes. Extracellular miRNAs function as chemical messengers to mediate cell-cell communication. In this review, we provide an update on canonical and non-canonical miRNA biogenesis pathways and various mechanisms underlying miRNA-mediated gene regulations. We also summarize the current knowledge of the dynamics of miRNA action and of the secretion, transfer, and uptake of extracellular miRNAs.
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            TGF-β and BMP signaling in osteoblast, skeletal development, and bone formation, homeostasis and disease

            Mengrui Wu, Guiqian Chen, YI-PING LI (2016)
            Transforming growth factor-beta (TGF-β) and bone morphogenic protein (BMP) signaling has fundamental roles in both embryonic skeletal development and postnatal bone homeostasis. TGF-βs and BMPs, acting on a tetrameric receptor complex, transduce signals to both the canonical Smad-dependent signaling pathway (that is, TGF-β/BMP ligands, receptors, and Smads) and the non-canonical-Smad-independent signaling pathway (that is, p38 mitogen-activated protein kinase/p38 MAPK) to regulate mesenchymal stem cell differentiation during skeletal development, bone formation and bone homeostasis. Both the Smad and p38 MAPK signaling pathways converge at transcription factors, for example, Runx2 to promote osteoblast differentiation and chondrocyte differentiation from mesenchymal precursor cells. TGF-β and BMP signaling is controlled by multiple factors, including the ubiquitin–proteasome system, epigenetic factors, and microRNA. Dysregulated TGF-β and BMP signaling result in a number of bone disorders in humans. Knockout or mutation of TGF-β and BMP signaling-related genes in mice leads to bone abnormalities of varying severity, which enable a better understanding of TGF-β/BMP signaling in bone and the signaling networks underlying osteoblast differentiation and bone formation. There is also crosstalk between TGF-β/BMP signaling and several critical cytokines’ signaling pathways (for example, Wnt, Hedgehog, Notch, PTHrP, and FGF) to coordinate osteogenesis, skeletal development, and bone homeostasis. This review summarizes the recent advances in our understanding of TGF-β/BMP signaling in osteoblast differentiation, chondrocyte differentiation, skeletal development, cartilage formation, bone formation, bone homeostasis, and related human bone diseases caused by the disruption of TGF-β/BMP signaling.
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              Emerging Roles of Vascular Cell Adhesion Molecule-1 (VCAM-1) in Immunological Disorders and Cancer

              Deok-Hoon Kong, Young Kim, Mi Kim … (2018)
              Tumor necrosis factor alpha (TNFα) is a pro-inflammatory cytokine that triggers the expression of inflammatory molecules, including other cytokines and cell adhesion molecules. TNFα induces the expression of intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 (VCAM-1). VCAM-1 was originally identified as a cell adhesion molecule that helps regulate inflammation-associated vascular adhesion and the transendothelial migration of leukocytes, such as macrophages and T cells. Recent evidence suggests that VCAM-1 is closely associated with the progression of various immunological disorders, including rheumatoid arthritis, asthma, transplant rejection, and cancer. This review covers the role and relevance of VCAM-1 in inflammation, and also highlights the emerging potential of VCAM-1 as a novel therapeutic target in immunological disorders and cancer.
              Article 0 comments Cited 226 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Rald Victor Maria Groven
                Carlos Julio Peniche Silva
                Elizabeth Rosado Balmayor
                Bart Nicolaas Jacobus van der Horst
                Martijn Poeze
                Taco Johan Blokhuis
                Martijn van Griensven
                Journal
                Journal ID (nlm-ta): J Orthop Translat
                Journal ID (iso-abbrev): J Orthop Translat
                Title: Journal of Orthopaedic Translation
                Publisher: Chinese Speaking Orthopaedic Society
                ISSN (Print): 2214-031X
                ISSN (Electronic): 2214-0328
                Publication date PMC-release: 31 August 2022
                Publication date Collection: November 2022
                Publication date (Electronic): 31 August 2022
                Volume: 37
                Pages: 1-11
                Affiliations
                [a ]Department of Cell Biology-Inspired Tissue Engineering, MERLN Institute for Technology-Inspired Regenerative Medicine, Maastricht University, Universiteitssingel 40, 6229 ER Maastricht, the Netherlands
                [b ]Division of Traumasurgery, Department of Surgery, Maastricht University Medical Center, P. Debyelaan 25, 6229 HX Maastricht, the Netherlands
                [c ]Department of Orthopaedic, Trauma, and Reconstructive Surgery, RWTH Aachen University Hospital, Pauwelsstraße 30, 52074 Aachen, Germany
                [d ]NUTRIM, School for Nutrition and Translational Research in Metabolism, Maastricht University, Universiteitssingel 40, 6229 ER Maastricht, the Netherlands
                Author notes
                [∗ ]Corresponding author. Universiteitssingel 40, 6229ER, Maastricht, the Netherlands. r.groven@ 123456maastrichtuniversity.nl
                Article
                Publisher Item ID: S2214-031X(22)00064-X
                DOI: 10.1016/j.jot.2022.07.002
                PMC ID: 9449672
                PubMed ID: 36128014
                SO-VID: bd08b94d-1065-44b4-a44e-90a042ff6da2
                Copyright © © 2022 The Authors
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 17 December 2021
                Date revision received : 1 July 2022
                Date accepted : 5 July 2022
                Categories
                Subject: Original Article

                Keywords: clinical parameters,fracture healing,gene expression,micrornas,mirna target analysis
                Data availability:
                Keywords: clinical parameters, fracture healing, gene expression, micrornas, mirna target analysis

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