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Osteoblast Differentiation and Activity in Skeletal Diseases 2.0
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Osteoblast Differentiation and Activity in Skeletal Diseases 2.0

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 January 2023) | Viewed by 12461

Special Issue Editors

Prof. Dr. Antonella Forlino

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Guest Editor
Department of Molecular Medicine, Unit of Biochemistry, University of Pavia, Pavia, Italy
Interests: osteogenesis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Pierre Moffatt

E-Mail Website
Guest Editor
Shriners Hospitals for Children – Canada and Department of Human Genetics, McGill University, Montréal, QC, Canada
Interests: bone physiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Bone is a complex tissue constituted by a mineral phase, hydroxyapatite, and an organic phase, mainly represented by collagen type I. Specialized cells are responsible for bone formation and remodeling, and their coordinated activity is necessary to maintain bone homeostasis. Osteoblasts are the bone-forming cells; osteocytes are the orchestrators of bone remodeling through regulation of the other bone cells’ activity, both by functioning as endocrine cells and by acting as mechanosensors; and osteoclasts are the bone-resorbing cells. The bone cellular compartment is a dynamic environment, and the cells’ crosstalk is fundamental to guarantee skeletal performance. A substantial body of evidence suggests that impairment in osteoblast differentiation and/or activity is responsible for several human diseases.

As volume one of the Special Issue “Osteoblast Differentiation and Activity in Skeletal Diseases” was successful, we are reopening this Issue in the International Journal of Molecular Sciences (https://www.mdpi.com/journal/ijms, ISSN 1422-0067, IF 5.924, JCR Category Q1). This second Issue will include a selection of research papers and reviews about various aspects of the molecular and cellular biology of osteoblasts, linking their impaired function to common and heritable skeletal diseases. How abnormal osteoblast differentiation and activity influence bone modelling and remodeling and extracellular matrix mineralization will also be addressed.

Prof. Dr. Antonella Forlino
Prof. Dr. Pierre Moffatt
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

  • osteoblast
  • secretory pathway
  • endoplasmic reticulum stress
  • signal transduction pathway
  • collagen type I
  • skeletal common disorders
  • skeletal heritable disorders
  • bone
  • matrix vesicles
  • osteoclasts

Published Papers (5 papers)

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Research

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13 pages, 3266 KiB  
Article
Biomechanical, Microstructural and Material Properties of Tendon and Bone in the Young Oim Mice Model of Osteogenesis Imperfecta
by Antoine Chretien, Malory Couchot, Guillaume Mabilleau and Catherine Behets
Int. J. Mol. Sci. 2022, 23(17), 9928; https://doi.org/10.3390/ijms23179928 - 01 Sep 2022
Cited by 4 | Viewed by 2060
Abstract
Osteogenesis imperfecta (OI) is a genetic disorder of connective tissue characterized by low bone mass and spontaneous fractures, as well as extra-skeletal manifestations, such as dental abnormalities, blue sclera, hearing loss and joint hypermobility. Tendon ruptures have been reported in OI patients. Here, [...] Read more.
Osteogenesis imperfecta (OI) is a genetic disorder of connective tissue characterized by low bone mass and spontaneous fractures, as well as extra-skeletal manifestations, such as dental abnormalities, blue sclera, hearing loss and joint hypermobility. Tendon ruptures have been reported in OI patients. Here, we characterized the biomechanical, structural and tissue material properties of bone and tendon in 5-week-old female osteogenesis imperfecta mice (oim), a validated model of severe type III OI, and compared these data with age- and sex-matched WT littermates. Oim tendons were less rigid and less resistant than those of WT mice. They also presented a significantly higher rate of pentosidine, without significant modification of enzymatic crosslinking. The oim bones were less resistant and avulsion fractures were evident at high tendinous stress areas. Alterations of trabecular and cortical bone microarchitectures were noticed in young female oim. Bone tissue material properties were also modified, with a less mature and more mineralized matrix in association with lower collagen maturity. Our data suggest that the tendon-to-bone unit is affected in young oim mice, which could explain tendon ruptures and bone fragility observed in OI patients. Full article
(This article belongs to the Special Issue Osteoblast Differentiation and Activity in Skeletal Diseases 2.0)
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16 pages, 1556 KiB  
Article
Impact of Fluid Flow Shear Stress on Osteoblast Differentiation and Cross-Talk with Articular Chondrocytes
by Paige V. Hinton, Katelyn J. Genoud, James O. Early, Fergal J. O’Brien and Oran D. Kennedy
Int. J. Mol. Sci. 2022, 23(16), 9505; https://doi.org/10.3390/ijms23169505 - 22 Aug 2022
Cited by 7 | Viewed by 3186
Abstract
Bone cells, in particular osteoblasts, are capable of communication with each other during bone growth and homeostasis. More recently it has become clear that they also communicate with other cell-types; including chondrocytes in articular cartilage. One way that this process is facilitated is [...] Read more.
Bone cells, in particular osteoblasts, are capable of communication with each other during bone growth and homeostasis. More recently it has become clear that they also communicate with other cell-types; including chondrocytes in articular cartilage. One way that this process is facilitated is by interstitial fluid movement within the pericellular and extracellular matrices. This stimulus is also an important mechanical signal in skeletal tissues, and is known to generate shear stresses at the micron-scale (known as fluid flow shear stresses (FFSS)). The primary aim of this study was to develop and characterize an in vitro bone–cartilage crosstalk system, to examine the effect of FFSS on these cell types. Specifically, we evaluated the response of osteoblasts and chondrocytes to FFSS and the effect of FFSS-induced soluble factors from the former, on the latter. This system will ultimately be used to help us understand the role of subchondral bone damage in articular cartilage degeneration. We also carried out a comparison of responses between cell lines and primary murine cells in this work. Our findings demonstrate that primary cells produce a more reliable and reproducible response to FFSS. Furthermore we found that at lower magnitudes , direct FFSS produces anabolic responses in both chondrocytes and osteoblasts, whereas higher levels produce more catabolic responses. Finally we show that exposure to osteoblast-derived factors in conditioned media experiments produced similarly catabolic changes in primary chondrocytes. Full article
(This article belongs to the Special Issue Osteoblast Differentiation and Activity in Skeletal Diseases 2.0)
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0 pages, 4245 KiB  
Article
The Osteogenesis Imperfecta Type V Mutant BRIL/IFITM5 Promotes Transcriptional Activation of MEF2, NFATc, and NR4A in Osteoblasts
by Vincent Maranda, Marie-Hélène Gaumond and Pierre Moffatt
Int. J. Mol. Sci. 2022, 23(4), 2148; https://doi.org/10.3390/ijms23042148 - 15 Feb 2022
Cited by 2 | Viewed by 2348
Abstract
BRIL (bone restricted ifitm-like; also known as IFITM5) is a transmembrane protein expressed in osteoblasts. Although its role in skeletal development and homeostasis is unknown, mutations in BRIL result in rare dominant forms of osteogenesis imperfecta. The pathogenic mechanism has been proposed to [...] Read more.
BRIL (bone restricted ifitm-like; also known as IFITM5) is a transmembrane protein expressed in osteoblasts. Although its role in skeletal development and homeostasis is unknown, mutations in BRIL result in rare dominant forms of osteogenesis imperfecta. The pathogenic mechanism has been proposed to be a gain-of or neomorphic function. To understand the function of BRIL and its OI type V mutant (MALEP BRIL) and whether they could activate signaling pathways in osteoblasts, we performed a luciferase reporter assay screen based on the activity of 26 transcription factors. When overexpressed in MC3T3-E1 and MLO-A5 cells, the MALEP BRIL activated the reporters dependent on MEF2, NFATc, and NR4A significantly more. Additional co-transfection experiments with MEF2C and NFATc1 and a number of their modulators (HDAC4, calcineurin, RCAN, FK506) confirmed the additive or synergistic activation of the pathways by MALEP, and suggested a coordinated regulation involving calcineurin. Endogenous levels of Nr4a members, as well as Ptgs2, were upregulated by MALEP BRIL. Y2H and co-immunoprecipitation indicated that BRIL interacted with CAML, but its contribution as the most upstream stimulator of the Ca2+-calcineurin-MEF2/NFATc cascade was not confirmed convincingly. Altogether the data presented provide the first ever readout to monitor for BRIL activity and suggest a potential gain-of-function causative effect for MALEP BRIL in OI type V, leading to perturbed signaling events and gene expression. Full article
(This article belongs to the Special Issue Osteoblast Differentiation and Activity in Skeletal Diseases 2.0)
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Review

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16 pages, 3342 KiB  
Review
Proteoglycans in Articular Cartilage and Their Contribution to Chondral Injury and Repair Mechanisms
by Lourdes Alcaide-Ruggiero, Ramón Cugat and Juan Manuel Domínguez
Int. J. Mol. Sci. 2023, 24(13), 10824; https://doi.org/10.3390/ijms241310824 - 28 Jun 2023
Cited by 7 | Viewed by 2367
Abstract
Proteoglycans are vital components of the extracellular matrix in articular cartilage, providing biomechanical properties crucial for its proper functioning. They are key players in chondral diseases, specifically in the degradation of the extracellular matrix. Evaluating proteoglycan molecules can serve as a biomarker for [...] Read more.
Proteoglycans are vital components of the extracellular matrix in articular cartilage, providing biomechanical properties crucial for its proper functioning. They are key players in chondral diseases, specifically in the degradation of the extracellular matrix. Evaluating proteoglycan molecules can serve as a biomarker for joint degradation in osteoarthritis patients, as well as assessing the quality of repaired tissue following different treatment strategies for chondral injuries. Despite ongoing research, understanding osteoarthritis and cartilage repair remains unclear, making the identification of key molecules essential for early diagnosis and effective treatment. This review offers an overview of proteoglycans as primary molecules in articular cartilage. It describes the various types of proteoglycans present in both healthy and damaged cartilage, highlighting their roles. Additionally, the review emphasizes the importance of assessing proteoglycans to evaluate the quality of repaired articular tissue. It concludes by providing a visual and narrative description of aggrecan distribution and presence in healthy cartilage. Proteoglycans, such as aggrecan, biglycan, decorin, perlecan, and versican, significantly contribute to maintaining the health of articular cartilage and the cartilage repair process. Therefore, studying these proteoglycans is vital for early diagnosis, evaluating the quality of repaired cartilage, and assessing treatment effectiveness. Full article
(This article belongs to the Special Issue Osteoblast Differentiation and Activity in Skeletal Diseases 2.0)
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18 pages, 2164 KiB  
Review
The Metabolic Features of Osteoblasts: Implications for Multiple Myeloma (MM) Bone Disease
by Oxana Lungu, Denise Toscani, Jessica Burroughs-Garcia and Nicola Giuliani
Int. J. Mol. Sci. 2023, 24(5), 4893; https://doi.org/10.3390/ijms24054893 - 03 Mar 2023
Cited by 1 | Viewed by 1822
Abstract
The study of osteoblast (OB) metabolism has recently received increased attention due to the considerable amount of energy used during the bone remodeling process. In addition to glucose, the main nutrient for the osteoblast lineages, recent data highlight the importance of amino acid [...] Read more.
The study of osteoblast (OB) metabolism has recently received increased attention due to the considerable amount of energy used during the bone remodeling process. In addition to glucose, the main nutrient for the osteoblast lineages, recent data highlight the importance of amino acid and fatty acid metabolism in providing the fuel necessary for the proper functioning of OBs. Among the amino acids, it has been reported that OBs are largely dependent on glutamine (Gln) for their differentiation and activity. In this review, we describe the main metabolic pathways governing OBs’ fate and functions, both in physiological and pathological malignant conditions. In particular, we focus on multiple myeloma (MM) bone disease, which is characterized by a severe imbalance in OB differentiation due to the presence of malignant plasma cells into the bone microenvironment. Here, we describe the most important metabolic alterations involved in the inhibition of OB formation and activity in MM patients. Full article
(This article belongs to the Special Issue Osteoblast Differentiation and Activity in Skeletal Diseases 2.0)
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