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Special Issue "Osteoclast Multinucleation Mechanisms"

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: 28 February 2020.

Special Issue Editor

Dr. Noriko Takegahara
E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA
Interests: cell biology; macrophage; osteoclast; polyploidization; cell fusion; bone metabolism

Special Issue Information

Dear Colleagues,

Osteoclasts are specialized, multinucleated, and giant cells that resorb bone. Multinucleation is a hallmark of mature osteoclasts. The importance of multinucleation in osteoclast formation is demonstrated by the impaired bone-resorbing activity of osteoclasts that cannot achieve multinucleation. A functional defect in osteoclasts results in abnormal bone homeostasis. Therefore, it is important to understand the molecular signaling and genetic programs that control osteoclast multinucleation to improve our understanding of osteoclast biology and provide a molecular basis for designing therapeutic strategies for bone remodeling diseases.

Osteoclasts are hematopoietic in origin and are derived from myeloid precursors that also give rise to macrophages. In the past few decades, important advances have been made in molecular characterization of osteoclast multinucleation. To date, a number of molecules as well as cellular mechanisms (cell adhesion, the actin-based cytoskeleton, membrane-associated elements, irregular cell cycle, and cell fusion) have been revealed to be required for osteoclast multinucleation.

This Special Issue aims to cover a selection of recent research topics and current review articles related to osteoclast multinucleation. Since multinucleation is also observed in macrophages, and multinucleated macrophages have potential similarities to osteoclasts, we also welcome research and reviews characterizing the mechanisms of macrophage multinucleation, which will give us additional insights into the mechanisms underlying osteoclast multinucleation. Up-to-date review articles, commentaries, and experimental papers are all welcome.

Dr. Noriko Takegahara
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. 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

  • osteoclast
  • macrophage
  • multinucleation
  • cell fusion
  • development
  • function
  • bone metabolism

Published Papers (2 papers)

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Research

Open AccessArticle
Pisidium coreanum Inhibits Multinucleated Osteoclast Formation and Prevents Estrogen-Deficient Osteoporosis
Int. J. Mol. Sci. 2019, 20(23), 6076; https://doi.org/10.3390/ijms20236076 - 02 Dec 2019
Abstract
Mollusks have served as important sources of human food and medicine for a long time. Raw Pisidium coreanum, a freshwater bivalve of the phylum Mollusca, is used in traditional therapies in parts of Asia. However, the therapeutic effects of Pisidium coreanum on [...] Read more.
Mollusks have served as important sources of human food and medicine for a long time. Raw Pisidium coreanum, a freshwater bivalve of the phylum Mollusca, is used in traditional therapies in parts of Asia. However, the therapeutic effects of Pisidium coreanum on bone diseases are not known. We investigated the functional roles of Pisidium coreanum in osteoporotic bone diseases. Pisidium coreanum inhibited the differentiation of bone marrow-derived monocytic cells into mature osteoclasts in vitro. The ovariectomized mice that received oral administration of Pisidium coreanum showed improvements in both trabecular and cortical bones. This preventive activity of Pisidium coreanum against bone loss was due to limited osteoclast maturation with reduced osteoclast surface extent in trabecular bone tissue. The formation of large multinucleated osteoclasts in vitro was significantly decreased in response to Pisidium coreanum, consistent with the reduced expression levels of osteoclast markers and fusion-related genes, such as NFATc1, p65, integrin αvβ3, DC-STAMP, OC-STAMP, Atp6v0d2, FAK, CD44, and MFR. These data suggest that Pisidium coreanum inhibits osteoclast differentiation by negatively regulating the fusion of mononuclear osteoclast precursors. Thus, our data demonstrate the ability of Pisidium coreanum to effectively prevent estrogen-deficient osteoporosis through inhibition of multinucleated osteoclast formation. Full article
(This article belongs to the Special Issue Osteoclast Multinucleation Mechanisms)
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Open AccessArticle
Osteoclast-Like Cells in Aneurysmal Disease Exhibit an Enhanced Proteolytic Phenotype
Int. J. Mol. Sci. 2019, 20(19), 4689; https://doi.org/10.3390/ijms20194689 - 21 Sep 2019
Abstract
Abdominal aortic aneurysm (AAA) is among the top 20 causes of death in the United States. Surgical repair is the gold standard for AAA treatment, therefore, there is a need for non-invasive therapeutic interventions. Aneurysms are more closely associated with the osteoclast-like catabolic [...] Read more.
Abdominal aortic aneurysm (AAA) is among the top 20 causes of death in the United States. Surgical repair is the gold standard for AAA treatment, therefore, there is a need for non-invasive therapeutic interventions. Aneurysms are more closely associated with the osteoclast-like catabolic degradation of the artery, rather than the osteoblast-like anabolic processes of arterial calcification. We have reported the presence of osteoclast-like cells (OLCs) in human and mouse aneurysmal tissues. The aim of this study was to examine OLCs from aneurysmal tissues as a source of degenerative proteases. Aneurysmal and control tissues from humans, and from the mouse CaPO4 and angiotensin II (AngII) disease models, were analyzed via flow cytometry and immunofluorescence for the expression of osteoclast markers. We found higher expression of the osteoclast markers tartrate-resistant acid phosphatase (TRAP), matrix metalloproteinase-9 (MMP-9), and cathepsin K, and the signaling molecule, hypoxia-inducible factor-1α (HIF-1α), in aneurysmal tissue compared to controls. Aneurysmal tissues also contained more OLCs than controls. Additionally, more OLCs from aneurysms express HIF-1α, and produce more MMP-9 and cathepsin K, than myeloid cells from the same tissue. These data indicate that OLCs are a significant source of proteases known to be involved in aortic degradation, in which the HIF-1α signaling pathway may play an important role. Our findings suggest that OLCs may be an attractive target for non-surgical suppression of aneurysm formation due to their expression of degradative proteases. Full article
(This article belongs to the Special Issue Osteoclast Multinucleation Mechanisms)
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