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Recent Molecular Advances in the Pathology and Therapeutics of Musculoskeletal Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 4232

Special Issue Editor

Dr. Cristina Sánchez-De-Diego

E-Mail Website
Guest Editor
Microtechnology, Medicine and Biology (MMB) Lab, Wisconsin Institutes for Medical Research, University of Wisconsin, Madison, WI 53705, USA
Interests: bone; osteocyte differentiation; bone marrow microenvironment; bone metabolism; oxidative stress; cancer research; bone metastasis; microfluidics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, “Recent Molecular Advances in the Pathology and Therapeutics of Musculoskeletal Disease”, offers a broad exploration of the latest breakthroughs in comprehending the immunopathology of diverse musculoskeletal diseases. This collection of articles sheds light on the pivotal role of the immune system in maintaining musculoskeletal homeostasis and contributing to the pathogenesis of disorders such as osteoporosis, rheumatoid arthritis, and bone metastasis, among others.

Delving into recent molecular advancements, this Special Issue unravels the intricate interplay among immune cells, cytokines, signaling molecules, and specific molecular pathways relevant to musculoskeletal diseases. Additionally, it unveils the discovery of novel therapeutic targets aimed at addressing the complexities of these conditions.

Our objective is to establish a comprehensive platform for researchers to present cutting-edge findings, fostering a deeper understanding of the immunopathology underlying musculoskeletal diseases. By doing so, we aim to for the development of targeted therapeutic strategies that improve patients’ outcomes in the realm of musculoskeletal health. Original research articles and critical reviews on the molecular advances of musculoskeletal disease are welcome.

Dr. Cristina Sánchez-De-Diego
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • osteoporosis

  • rheumatoid arthritis
  • bone metastasis
  • cytokines
  • immunopathology
  • immunotherapy
  • musculoskeletal

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

12 pages, 3704 KiB  
Article
IL-17RA Signaling in Prx1+ Mesenchymal Cells Influences Fracture Healing in Mice
by Joseph L. Roberts, David Kapfhamer, Varsha Devarapalli and Hicham Drissi
Int. J. Mol. Sci. 2024, 25(7), 3751; https://doi.org/10.3390/ijms25073751 - 28 Mar 2024
Cited by 2 | Viewed by 1505
Abstract
Fracture healing is a complex series of events that requires a local inflammatory reaction to initiate the reparative process. This inflammatory reaction is important for stimulating the migration and proliferation of mesenchymal progenitor cells from the periosteum and surrounding tissues to form the [...] Read more.
Fracture healing is a complex series of events that requires a local inflammatory reaction to initiate the reparative process. This inflammatory reaction is important for stimulating the migration and proliferation of mesenchymal progenitor cells from the periosteum and surrounding tissues to form the cartilaginous and bony calluses. The proinflammatory cytokine interleukin (IL)-17 family has gained attention for its potential regenerative effects; however, the requirement of IL-17 signaling within mesenchymal progenitor cells for normal secondary fracture healing remains unknown. The conditional knockout of IL-17 receptor a (Il17ra) in mesenchymal progenitor cells was achieved by crossing Il17raF/F mice with Prx1-cre mice to generate Prx1-cre; Il17raF/F mice. At 3 months of age, mice underwent experimental unilateral mid-diaphyseal femoral fractures and healing was assessed by micro-computed tomography (µCT) and histomorphometric analyses. The effects of IL-17RA signaling on the osteogenic differentiation of fracture-activated periosteal cells was investigated in vitro. Examination of the intact skeleton revealed that the conditional knockout of Il17ra decreased the femoral cortical porosity but did not affect any femoral trabecular microarchitectural indices. After unilateral femoral fractures, Il17ra conditional knockout impacted the cartilage and bone composition of the fracture callus that was most evident early in the healing process (day 7 and 14 post-fracture). Furthermore, the in vitro treatment of fracture-activated periosteal cells with IL-17A inhibited osteogenesis. This study suggests that IL-17RA signaling within Prx1+ mesenchymal progenitor cells can influence the early stages of endochondral ossification during fracture healing. Full article
(This article belongs to the Special Issue Recent Molecular Advances in the Pathology and Therapeutics of Musculoskeletal Disease)
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10 pages, 4045 KiB  
Article
Administration of Recombinant TAPBPL Protein Ameliorates Collagen-Induced Arthritis in Mice
by Zhenzhen Zhang, Jin Zhao, Kuan Chen Lai and Laijun Lai
Int. J. Mol. Sci. 2023, 24(18), 13772; https://doi.org/10.3390/ijms241813772 - 7 Sep 2023
Cited by 1 | Viewed by 2004
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease distinguished by synovial hyperplasia and a progressive destruction of joints. T cells are critical players in the pathogenesis of RA. We have previously identified a novel immune checkpoint molecule, TAPBPL, that inhibits T cell [...] Read more.
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease distinguished by synovial hyperplasia and a progressive destruction of joints. T cells are critical players in the pathogenesis of RA. We have previously identified a novel immune checkpoint molecule, TAPBPL, that inhibits T cell functions in vitro. As a model for human RA, we investigated the ability of the TAPBPL protein to ameliorate collagen type II (CII)-induced arthritis (CIA) in mice that were injected with recombinant TAPBPL or a control protein. The mice were analyzed for CIA development, immune cells, and their responses. We found that TAPBPL protein significantly decreased CIA incidence and reduced clinical and pathological arthritis scores, which were related to a lower number of activated CD4 T cells but a greater number of regulatory T cells (Tregs) in the spleen, and a reduction of Th1/Th17 inflammatory cytokines in the joints and serum. Importantly, TAPBPL protein inhibited CII-specific T cell growth and Th1 and Th17 cytokine expression and reduced the production of CII autoantibodies in the serum. Our results suggest that TAPBPL protein can ameliorate CIA in mice and has the potential to be used in the treatment of patients with RA. Full article
(This article belongs to the Special Issue Recent Molecular Advances in the Pathology and Therapeutics of Musculoskeletal Disease)
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