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Molecular and Cellular Mechanisms of Osteoarthritis
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Molecular and Cellular Mechanisms of Osteoarthritis

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

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 3693

Special Issue Editors

Dr. Michael J. Jurynec

E-Mail Website
Guest Editor
Department of Orthopaedics, University of Utah, Salt Lake City, UT 84108, USA
Interests: arthritis; osteoarthritis; mouse models; zebrafish; genetics; human genetics; inflammation; cartilage; chondrocytes
Dr. Nikolas Kazmers

E-Mail Website
Guest Editor
Department of Orthopaedics, University of Utah, Salt Lake City, UT 84108, USA
Interests: Osteoarthritis; genetics; hand osteoarthritis

Special Issue Information

Dear Colleagues,

Osteoarthritis (OA) is a debilitating disease characterized by the loss of joint space, the degeneration of cartilage at articular surfaces, the remodeling of bone and other joint tissues, and low-grade inflammation. It is the major cause of disability in the aged population, affecting >32 million (11%) adults in the US. No cure for OA exists. There is not a single disease-modifying OA drug available. With the exception of surgical intervention such as joint replacement, therapies are solely palliative. We do not know the molecular pathways that are rate-limiting in the disease process and that need to be targeted for effective therapies.

This Special Issue is focused on the cellular, molecular, and genetic research on osteoarthritis. It will include original articles as well as reviews on all aspects related to the progress and current knowledge of the molecular and cellular mechanisms of osteoarthritis.

Dr. Michael J. Jurynec
Dr. Nikolas Kazmers 
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. 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

  • osteoarthritis
  • degenerative arthritis
  • degenerative joint disease
  • inflammation
  • pharma-cology
  • apoptosis
  • signal transduction
  • chondrocytes
  • genetics
  • mouse models

Published Papers (1 paper)

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Research

18 pages, 4093 KiB  
Article
Role of GDF15/MAPK14 Axis in Chondrocyte Senescence as a Novel Senomorphic Agent in Osteoarthritis
by Pei-Wei Weng, Narpati Wesa Pikatan, Syahru Agung Setiawan, Vijesh Kumar Yadav, Iat-Hang Fong, Chia-Hung Hsu, Chi-Tai Yeh and Wei-Hwa Lee
Int. J. Mol. Sci. 2022, 23(13), 7043; https://doi.org/10.3390/ijms23137043 - 24 Jun 2022
Cited by 10 | Viewed by 3324
Abstract
Osteoarthritis (OA) is most prevalent in older individuals and exerts a heavy social and economic burden. However, an effective and noninvasive approach to OA treatment is currently not available. Chondrocyte senescence has recently been proposed as a key pathogenic mechanism in the etiology [...] Read more.
Osteoarthritis (OA) is most prevalent in older individuals and exerts a heavy social and economic burden. However, an effective and noninvasive approach to OA treatment is currently not available. Chondrocyte senescence has recently been proposed as a key pathogenic mechanism in the etiology of OA. Furthermore, senescent chondrocytes (SnCCs) can release various proinflammatory cytokines, proteolytic enzymes, and other substances known as the senescence-associated secretory phenotype (SASP), allowing them to connect with surrounding cells and induce senesce. Studies have shown that the pharmacological elimination of SnCCs slows the progression of OA and promotes regeneration. Growth differentiation factor 15 (GDF15), a member of the tumor growth factor (TGF) superfamily, has recently been identified as a possible aging biomarker and has been linked to a variety of clinical conditions, including coronary artery disease, diabetes, and multiple cancer types. Thus, we obtained data from a publicly available single-cell sequencing RNA database and observed that GDF15, a critical protein in cellular senescence, is highly expressed in early OA. In addition, GDF15 is implicated in the senescence and modulation of MAPK14 in OA. Tissue and synovial fluid samples obtained from OA patients showed overexpression of GDF15. Next, we treated C20A4 cell lines with interleukin (IL)-1β with or without shGDF15 then removed the conditioned medium, and cultured C20A4 and HUVEC cell lines with the aforementioned media. We observed that C20A4 cells treated with IL-1β exhibited increased GDF15 secretion and that chondrocytes cultured with media derived from IL-1β–treated C20A4 exhibited senescence. HUVEC cell migration and tube formation were enhanced after culturing with IL-1β-treated chondrocyte media; however, decreased HUVEC cell migration and tube formation were noted in HUVEC cells cultured with GDF15-loss media. We tested the potential of inhibiting GDF15 by using a GDF15 neutralizing antibody, GDF15-nAb. GDF15-nAb exerted a similar effect, resulting in the molecular silencing of GDF15 in vivo and in vitro. Our results reveal that GDF15 is a driver of SnCCs and can contribute to OA progression by inducing angiogenesis. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Osteoarthritis)
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