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Cells
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Frontiers in Chondrocyte Biology
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Frontiers in Chondrocyte Biology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 9029

Special Issue Editor

Dr. Jennifer H. Jonason

E-Mail Website
Guest Editor
Department of Orthopaedics and Rehabilitation, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, New York 14642, USA
Interests: cartilage biology; osteoarthritis; endochondral bone formation

Special Issue Information

Dear Colleagues,

The chondrocyte, a mesenchymal progenitor derivative, is the sole cell type found in vertebrate hyaline growth plates and articular cartilage tissues. It is responsible for the development and maintenance of the cartilage extracellular matrix, and responds to both molecular and mechanical cues. Depending on the cues received, the chondrocyte may proliferate, exit the cell cycle, differentiate into a hypertrophic state, or undergo cell death. Recent evidence also suggests that during development, the chondrocyte can transdifferentiate into a bone-forming osteoblast. These phenotypic changes by the chondrocyte govern endochondral bone formation during development as well as during fracture repair. While adult articular chondrocytes residing in the unmineralized articular cartilage are a mostly quiescent cell population, evidence suggests they can re-enter the cell cycle and undergo hypertrophy during the pathogenesis of osteoarthritis, likely contributing to degeneration of their matrix. The underlying mechanisms governing the chondrocyte phenotype involve signaling events that regulate gene expression as well as cellular processes such as metabolism, mitochondrial function, ER integrity, and autophagy, among others. In this Special Issue entitled, “Frontiers in Chondrocyte Biology,” we invite submissions on the molecular and biomechanical regulation of the chondrocyte phenotype during development, bone repair, cartilage homeostasis, and joint pathogenesis.

Dr. Jennifer H. Jonason
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. Cells is an international peer-reviewed open access semimonthly 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

  • chondrocyte
  • cartilage
  • growth plate
  • fracture repair
  • osteoarthritis
  • tissue homeostasis
  • aging
  • differentiation
  • hypertrophy
  • proliferation
  • apoptosis
  • autophagy
  • signal transduction
  • metabolism
  • mitochondria

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Published Papers (3 papers)

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Research

15 pages, 2532 KiB  
Article
The Critical Role of Hypoxia in the Re-Differentiation of Human Articular Chondrocytes
by Carlos Martinez-Armenta, Carlos Suarez-Ahedo, Anell Olivos-Meza, María C. Camacho-Rea, Laura E. Martínez-Gómez, Guadalupe Elizabeth Jimenez-Gutierrez, Gabriela A. Martínez-Nava, Luis E. Gomez-Quiroz, Carlos Pineda and Alberto López-Reyes
Cells 2022, 11(16), 2553; https://doi.org/10.3390/cells11162553 - 17 Aug 2022
Cited by 2 | Viewed by 2412
Abstract
The preservation of the chondrogenic phenotype and hypoxia-related physiological microenvironment are major challenges in the 2D culture of primary human chondrocytes. To address this problem, we develop a 3D culture system generating scaffold-free spheroids from human chondrocytes. Our results highlight the chondrogenic potential [...] Read more.
The preservation of the chondrogenic phenotype and hypoxia-related physiological microenvironment are major challenges in the 2D culture of primary human chondrocytes. To address this problem, we develop a 3D culture system generating scaffold-free spheroids from human chondrocytes. Our results highlight the chondrogenic potential of cultured human articular chondrocytes in a 3D system combined with hypoxia independently of the cartilage source. After 14 days of culture, we developed spheroids with homogenous diameter and shape from hyaline cartilage donors. Spheroids generated in hypoxia showed a significantly increased glycosaminoglycans synthesis and up-regulated the expression of SOX9, ACAN, COL2A1, COMP, and SNAI1 compared to those obtained under normoxic conditions. Therefore, we conclude that spheroids developed under hypoxic conditions modulate the expression of chondrogenesis-related genes and native tissue features better than 2D cultures. Thus, this scaffold-free 3D culture system represents a novel in vitro model that can be used for cartilage biology research. Full article
(This article belongs to the Special Issue Frontiers in Chondrocyte Biology)
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17 pages, 4111 KiB  
Article
Identification of N-Glycoproteins of Knee Cartilage from Adult Osteoarthritis and Kashin-Beck Disease Based on Quantitative Glycoproteomics, Compared with Normal Control Cartilage
by Jing Han, Huan Deng, Yizhen Lyu, Xiang Xiao, Yan Zhao, Jiaxin Liu, Ziwei Guo, Xuan Liu, Lichun Qiao, Hang Gao and Mikko Juhani Lammi
Cells 2022, 11(16), 2513; https://doi.org/10.3390/cells11162513 - 12 Aug 2022
Cited by 9 | Viewed by 2811
Abstract
Glycoproteins are involved in the development of many diseases, while the type and content of N-glycoproteins in the cartilage of osteoarthritis (OA) and Kashin–Beck disease (KBD) are still unclear. This research aims to identify N-glycoproteins in knee cartilage patients with OA and KBD [...] Read more.
Glycoproteins are involved in the development of many diseases, while the type and content of N-glycoproteins in the cartilage of osteoarthritis (OA) and Kashin–Beck disease (KBD) are still unclear. This research aims to identify N-glycoproteins in knee cartilage patients with OA and KBD compared with normal control (N) adults. The cartilage samples were collected from gender- and age-matched OA (n = 9), KBD (n = 9) patients, and N (n = 9) adults. Glycoproteomics and label-free liquid chromatography-tandem mass spectrometry (LC-MS/MS) obtained N-glycoproteins of KBD and OA. A total of 594 N-glycoproteins and 1146 N-glycosylation peptides were identified. The identified data were further compared and analyzed with Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Protein–Protein Interactions (PPI). Pairwise comparison of the glycoproteins detected in the three groups showed that integrin beta-1 (ITGB1), collagen alpha-1 (II) chain (COL2A1), collagen alpha-1 (VII) chain (COL7A1), carbohydrate sulfotransferase 3 (CHST-3), carbohydrate sulfotransferase 4 (CHST-4), thrombospondin 2 (THBS2), bone morphogenetic protein 8A (BMP8A), tenascin-C (TNC), lysosome-associated membrane protein (LAMP2), and beta-glucuronidase (GUSB) were significantly differentially expressed. GO results suggested N-glycoproteins mainly belonged to protein metabolic process, single-multicellular and multicellular organism process, cell adhesion, biological adhesion, and multicellular organism development. KEGG and PPI results revealed that key N-glycoproteins were closely related to pathways for OA and KBD, such as phagosome, ECM-receptor interaction, lysosome, focal adhesion, protein digestion, and absorption. These results reflected glycoprotein expression for OA and KBD in the process of ECM degradation, material transport, cell–cell or cell–ECM interaction, and information transduction. These key significantly differentially expressed N-glycoproteins and pathways lead to the degeneration and degradation of the cartilage of OA and KBD mainly by disrupting the synthesis and catabolism of basic components of ECM and chondrocytes and interfering with the transfer of material or information. The key N-glycoproteins or pathways in this research are potential targets for pathological mechanisms and therapies of OA and KBD. Full article
(This article belongs to the Special Issue Frontiers in Chondrocyte Biology)
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18 pages, 2066 KiB  
Article
Identification of Transcription Factors Responsible for a Transforming Growth Factor-β-Driven Hypertrophy-like Phenotype in Human Osteoarthritic Chondrocytes
by Nathalie G. M. Thielen, Margot Neefjes, Elly L. Vitters, Henk M. van Beuningen, Arjen B. Blom, Marije I. Koenders, Peter L. E. M. van Lent, Fons A. J. van de Loo, Esmeralda N. Blaney Davidson, Arjan P. M. van Caam and Peter M. van der Kraan
Cells 2022, 11(7), 1232; https://doi.org/10.3390/cells11071232 - 5 Apr 2022
Cited by 11 | Viewed by 3084
Abstract
During osteoarthritis (OA), hypertrophy-like chondrocytes contribute to the disease process. TGF-β’s signaling pathways can contribute to a hypertrophy(-like) phenotype in chondrocytes, especially at high doses of TGF-β. In this study, we examine which transcription factors (TFs) are activated and involved in TGF-β-dependent induction [...] Read more.
During osteoarthritis (OA), hypertrophy-like chondrocytes contribute to the disease process. TGF-β’s signaling pathways can contribute to a hypertrophy(-like) phenotype in chondrocytes, especially at high doses of TGF-β. In this study, we examine which transcription factors (TFs) are activated and involved in TGF-β-dependent induction of a hypertrophy-like phenotype in human OA chondrocytes. We found that TGF-β, at levels found in synovial fluid in OA patients, induces hypertrophic differentiation, as characterized by increased expression of RUNX2, COL10A1, COL1A1, VEGFA and IHH. Using luciferase-based TF activity assays, we observed that the expression of these hypertrophy genes positively correlated to SMAD3:4, STAT3 and AP1 activity. Blocking these TFs using specific inhibitors for ALK-5-induced SMAD signaling (5 µM SB-505124), JAK-STAT signaling (1 µM Tofacitinib) and JNK signaling (10 µM SP-600125) led to the striking observation that only SB-505124 repressed the expression of hypertrophy factors in TGF-β-stimulated chondrocytes. Therefore, we conclude that ALK5 kinase activity is essential for TGF-β-induced expression of crucial hypertrophy factors in chondrocytes. Full article
(This article belongs to the Special Issue Frontiers in Chondrocyte Biology)
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