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Frontiers in Musculoskeletal and Neuromusculoskeletal Regenerative Medicine

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A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 8830

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Special Issue Editors

Dr. Federica Francesca Masieri

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Guest Editor

Biotechnology Unit, Life Sciences, School of (EAST) Engineering, Arts, Science & Technology, University of Suffolk, Ipswich IP41QJ, UK
Interests: musculoskeletal regeneration; stem cells; cartilage; synovium; translational research; biophysical cues

Dr. Aida Rajic

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Guest Editor

Biotechnology Unit, Life Sciences, School of (EAST) Engineering, Arts, Science & Technology, University of Suffolk, Ipswich IP41QJ, UK
Interests: CNS regeneration; CNS development; stem cells; steroid hormones

Special Issue Information

Dear Colleagues,

It is our pleasure to bring to your attention the upcoming Special Issue “Frontiers in Musculoskeletal and Neuromusculoskeletal Regenerative Medicine”, which is to be published in Biomolecules by the end of 2021. This Special Issue aims to discuss and present novel research in the area of musculoskeletal (MSK) regeneration, as well as on the contribution of the neuronal system to key MSK regenerative processes. We welcome both basic and translational research evidence, encompassing emerging and promising in vitro, quasi vivo, and pre-clinical models. We are also interested in receiving high-quality systematic reviews or meta-analyses that could complement and advance knowledge in the field. The research articles should contain novel findings and follow the format suggested for Biomolecules.

The submission deadline is 20 November 2021. Please share this announcement to other colleagues that you feel might be interested in contributing.

Dr. Federica Francesca Masieri
Dr. Aida Rajic
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

musculoskeletal regeneration;

stem cells;

neuronal cues;

musculoskeletal tissue development and engineering

Published Papers (3 papers)

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Research

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15 pages, 7060 KiB

Open AccessArticle

Fibrin with Laminin-Nidogen Reduces Fibrosis and Improves Soft Palate Regeneration Following Palatal Injury

by Doris H. Rosero Salazar, René E. M. van Rheden, Manon van Hulzen, Paola L. Carvajal Monroy, Frank A. D. T. G. Wagener and Johannes W. Von den Hoff

Biomolecules 2021, 11(10), 1547; https://doi.org/10.3390/biom11101547 - 19 Oct 2021

Cited by 3 | Viewed by 2103

Abstract

This study aimed to analyze the effects of fibrin constructs enhanced with laminin-nidogen, implanted in the wounded rat soft palate. Fibrin constructs with and without laminin-nidogen were implanted in 1 mm excisional wounds in the soft palate of 9-week-old rats and compared with the wounded soft palate without implantation. Collagen deposition and myofiber formation were analyzed at days 3, 7, 28 and 56 after wounding by histochemistry. In addition, immune staining was performed for a-smooth muscle actin (a-SMA), myosin heavy chain (MyHC) and paired homeobox protein 7 (Pax7). At day 56, collagen areas were smaller in both implant groups (31.25 ± 7.73% fibrin only and 21.11 ± 6.06% fibrin with laminin-nidogen)) compared to the empty wounds (38.25 ± 8.89%, p < 0.05). Moreover, the collagen area in the fibrin with laminin-nidogen group was smaller than in the fibrin only group (p ˂ 0.05). The areas of myofiber formation in the fibrin only group (31.77 ± 10.81%) and fibrin with laminin-nidogen group (43.13 ± 10.39%) were larger than in the empty wounds (28.10 ± 11.68%, p ˂ 0.05). Fibrin-based constructs with laminin-nidogen reduce fibrosis and improve muscle regeneration in the wounded soft palate. This is a promising strategy to enhance cleft soft palate repair and other severe muscle injuries. Full article

(This article belongs to the Special Issue Frontiers in Musculoskeletal and Neuromusculoskeletal Regenerative Medicine)

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13 pages, 3386 KiB

Open AccessCommunication

Partial Ablation of Non-Myogenic Progenitor Cells as a Therapeutic Approach to Duchenne Muscular Dystrophy

by Zhanguo Gao, Aiping Lu, Alexes C. Daquinag, Yongmei Yu, Matthieu Huard, Chieh Tseng, Xueqin Gao, Johnny Huard and Mikhail G. Kolonin

Biomolecules 2021, 11(10), 1519; https://doi.org/10.3390/biom11101519 - 15 Oct 2021

Cited by 3 | Viewed by 2654

Abstract

Duchenne muscular dystrophy (DMD), caused by the loss of dystrophin, remains incurable. Reduction in muscle regeneration with DMD is associated with the accumulation of fibroadipogenic progenitors (FAPs) differentiating into myofibroblasts and leading to a buildup of the collagenous tissue aggravating DMD pathogenesis. Mesenchymal stromal cells (MSCs) expressing platelet-derived growth factor receptors (PDGFRs) are activated in muscle during DMD progression and give rise to FAPs promoting DMD progression. Here, we hypothesized that muscle dysfunction in DMD could be delayed via genetic or pharmacologic depletion of MSC-derived FAPs. In this paper, we test this hypothesis in dystrophin-deficient mdx mice. To reduce fibro/adipose infiltration and potentiate muscle progenitor cells (MPCs), we used a model for inducible genetic ablation of proliferating MSCs via a suicide transgene, viral thymidine kinase (TK), expressed under the Pdgfrb promoter. We also tested if MSCs from fat tissue, the adipose stromal cells (ASCs), contribute to FAPs and could be targeted in DMD. Pharmacological ablation was performed with a hunter-killer peptide D-CAN targeting ASCs. MSC depletion with these approaches resulted in increased endurance, measured based on treadmill running, as well as grip strength, without significantly affecting fibrosis. Although more research is needed, our results suggest that depletion of pathogenic MSCs mitigates muscle damage and delays the loss of muscle function in mouse models of DMD. Full article

(This article belongs to the Special Issue Frontiers in Musculoskeletal and Neuromusculoskeletal Regenerative Medicine)

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16 pages, 1400 KiB

Open AccessSystematic Review

Role of Regulatory T Cells in Skeletal Muscle Regeneration: A Systematic Review

by Jaciara F. G. Gama, Rayza D. Romualdo, Mayara L. de Assis, Luana M. de Oliveira, Thereza Quírico-Santos, Luiz A. Alves and Jussara Lagrota-Candido

Biomolecules 2022, 12(6), 817; https://doi.org/10.3390/biom12060817 - 11 Jun 2022

Cited by 2 | Viewed by 2916

Abstract

Muscle injuries are frequent in individuals with genetic myopathies and in athletes. Skeletal muscle regeneration depends on the activation and differentiation of satellite cells present in the basal lamina of muscle fibers. The skeletal muscle environment is critical for repair, metabolic and homeostatic function. Regulatory T cells (Treg) residing within skeletal muscle comprise a distinct and special cell population that modifies the inflammatory environment by secreting cytokines and amphiregulin, an epidermal growth factor receptor (EGFR) ligand that acts directly upon satellite cells, promoting tissue regeneration. This systematic review summarizes the current knowledge regarding the role of Treg in muscle repair and discusses their therapeutic potential in skeletal muscle injuries. A bibliographic search was carried out using the terms Treg and muscle regeneration and repair, covering all articles up to April 2021 indexed in the PubMed and EMBASE databases. The search included only published original research in human and experimental animal models, with further data analysis based on the PICO methodology, following PRISMA definitions and Cochrane guidelines. Full article

(This article belongs to the Special Issue Frontiers in Musculoskeletal and Neuromusculoskeletal Regenerative Medicine)

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