Special Issue "Articular Cells and Tissues in Health and Osteoarthritis"

A special issue of Journal of Functional Morphology and Kinesiology (ISSN 2411-5142).

Deadline for manuscript submissions: closed (30 September 2017).

Special Issue Editors

Guest Editor
Prof. Dr. Alexandrina Ferreira Mendes Website E-Mail
Faculty of Pharmacy and Centre for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
Interests: aging; arthritis; chondrocyte biology; cartilage; inflammation; metabolic osteoarthritis; pharmacology
Guest Editor
Prof. Dr. Charles J. Malemud Website E-Mail
Department of Medicine, CASE School of Medicine, Cleveland, United States
Interests: inflammation; apoptosis, arthritis, chondrocytes, matrix metalloproteinases, signal transduction; pro-inflammatory; anti-inflammatory & amp; anabolic cytokines

Special Issue Information

Dear Colleagues,

Osteoarthritis (OA), the most frequent musculoskeletal disease and a huge socio-economic burden, has recently been defined as “a progressive disease of synovial joints that represents failed repair of joint damage that results from stresses that may be initiated by an abnormality in any of the synovial joint tissues, including articular cartilage, subchondral bone, ligaments, menisci (when present), periarticular muscles, peripheral nerves, or synovium”. This highlights the complex nature of OA etiology, likely defining a heterogeneous group of conditions that differ in etiopathogenesis and clinical course, but share a final outcome characterized by joint destruction. Current knowledge regarding the cellular and molecular mechanisms that drive joint destruction is still limited. Hence, a better understanding of the physiology of all joint tissues and how they influence each other, as well as of the mechanisms by which each joint tissue contributes to OA development and progression, is essential for the develoment of new more effective therapies.

This objective, thus, pertains both to basic and clinical research relating to articular cartilage, bone, synovial membrane, menisci, tendons, ligaments, muscles and peripheral nerves. This Special Issue “Articular Cells and Tissues in Health and Osteoarthritis”, aims at contributing to highlight the role of the various articular tissues and cells in health and OA pathogenesis and so, welcomes original articles and current reviews that tackle these subjects, either from a basic research or clinical point of view.

Dr. Alexandrina Ferreira Mendes
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 papers will be 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. Journal of Functional Morphology and Kinesiology is an international peer-reviewed open access quarterly 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 1000 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

  • osteoarthritis
  • joint function
  • articular cartilage/chondrocyte
  • synovium/synovial membrane
  • subchondral bone
  • periarticular muscle
  • ligament
  • tendon
  • meniscus
  • peripheral nerve and neurotransmitter

Published Papers (2 papers)

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Research

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Open AccessArticle
Hyperglycemia and Hyperinsulinemia-Like Conditions Independently Induce Inflammatory Responses in Human Chondrocytes
J. Funct. Morphol. Kinesiol. 2017, 2(2), 15; https://doi.org/10.3390/jfmk2020015 - 16 May 2017
Abstract
To elucidate the mechanisms by which type 2 Diabetes Mellitus (DM2) constitutes a risk factor for the development and progression of osteoarthritis (OA), this work determined whether high glucose and/or high insulin, the hallmarks of DM2, are capable of activating the transcription factor, [...] Read more.
To elucidate the mechanisms by which type 2 Diabetes Mellitus (DM2) constitutes a risk factor for the development and progression of osteoarthritis (OA), this work determined whether high glucose and/or high insulin, the hallmarks of DM2, are capable of activating the transcription factor, Nuclear Factor-κB (NF-κB), which plays a critical role in OA by inducing the expression of pro-inflammatory and catabolic genes. For this, we analyzed NF-κB activation by measuring the nuclear levels of p65 by western blot. As readouts of NF-κB activity, Interleukin-1β, Tumor Necrosis Factor-α, and inducible nitric oxide synthase (iNOS) expression were analyzed by real time RT-PCR and western blot. Culture of the human chondrocytic cell line, C28-I2, in high glucose (30 mM) increased nuclear NF-κB p65 levels in a time-dependent manner, relative to cells cultured in medium containing 10 mM glucose (regular culture medium). High glucose-induced NF-κB activation was inhibited by co-treatment with its specific inhibitor, Bay 11-7082, 5 µM. Culture of primary human chondrocytes under high glucose for 24 h increased IL-1β and TNF-α mRNA levels by 97% (p = 0.0066) and 85% (p = 0.0045), respectively, while iNOS mRNA and protein levels and NO production increased by 61% (p = 0.0017), 148% (p = 0.0089), and 70% (p = 0.049), respectively, relative to chondrocytes maintained in 10 mM glucose. Treatment of chondrocytic cells with 100 nM insulin was also sufficient to increase nuclear NF-κB p65 levels, independently of the glucose concentration in the culture medium. This study shows that hyperglycemia and hyperinsulinemia are independently sufficient to induce inflammatory responses in human chondrocytes, namely by activating NF-κB. This can be a relevant mechanism by which DM type 2 and other conditions associated with impaired glucose and insulin homeostasis, like obesity and the metabolic syndrome, contribute to the development and progression of OA. Full article
(This article belongs to the Special Issue Articular Cells and Tissues in Health and Osteoarthritis)
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Review

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Open AccessReview
A Role for Soluble IL-6 Receptor in Osteoarthritis
J. Funct. Morphol. Kinesiol. 2017, 2(3), 27; https://doi.org/10.3390/jfmk2030027 - 02 Aug 2017
Cited by 9
Abstract
Interleukin-6 (IL-6) is one of several pro-inflammatory cytokines present at elevated levels in the synovial fluid of individuals with confirmed clinical diagnosis of rheumatoid arthritis (RA) and osteoarthritis (OA). The mechanism of action of IL-6 was shown to involve its capacity to interact [...] Read more.
Interleukin-6 (IL-6) is one of several pro-inflammatory cytokines present at elevated levels in the synovial fluid of individuals with confirmed clinical diagnosis of rheumatoid arthritis (RA) and osteoarthritis (OA). The mechanism of action of IL-6 was shown to involve its capacity to interact with a membrane-bound IL-6 receptor (mIL-6Rα), also known as the “classical” IL-6 pathway, or through its interaction with a soluble IL-6 receptor (sIL-6R) termed the “trans-signaling” pathway. Activation of downstream signaling is transduced via these IL-6 receptors and principally involves the Janus Kinase/Signal Transduction and Activators of Transcription (JAK/STAT) signaling pathway that is further regulated by glycoprotein-130 (gp130) interacting with the IL-6/mIL-6R complex. Phosphorylation of STAT proteins via JAK activation facilitates STAT proteins to act as transcription factors in inflammation. However, the biological function(s) of the sIL-6R in human chondrocytes requires further elucidation, although we previously showed that exogenous sIL-6R significantly suppressed the synthesis of neutrophil gelatinase-associated lipocalin (NGAL) in the immortalized line of human chondrocytes, C28/I2. NGAL was shown to regulate the activity of matrix metalloproteinase-9 (MMP-9), whose activity is crucial in OA for the destruction of articular cartilage. The “shedding” of sIL-6R from the plasma membrane is carried out by a family of enzymes known as A Distintegrin and Metalloproteinase (ADAM), which are also elevated in OA. In this paper, we have systematically reviewed the role played by IL-6 in OA. We have proposed that sIL-6R may be an important target for future drug development in OA by ameliorating cartilage extracellular protein degradation. Full article
(This article belongs to the Special Issue Articular Cells and Tissues in Health and Osteoarthritis)
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