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Cells
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Signaling Pathways and Membrane Trafficking in Osteoclasts
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Signaling Pathways and Membrane Trafficking in Osteoclasts

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 4906

Special Issue Editor

Prof. Dr. Takayuki Tsukuba

E-Mail Website
Guest Editor
Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan
Interests: membrane trafficking; lysosome biogenesis; cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

 

Osteoclasts are bone-resorbing giant cells that have multinucleated formations. The mechanisms of osteoclast differentiation are strictly controlled by various signaling pathways. In addition, a characteristic of osteoclast differentiation is the formation of specific membrane called “ruffled border”. Therefore, osteoclast differentiation is closely regulated by various intracellular signaling pathways and membrane trafficking mechanisms.

This Special Issue on “Signaling Pathways and Membrane Trafficking in Osteoclasts” aims to gather high-quality research articles, review articles, and communications (including opinion and hypothesis papers) in all fields of osteoclasts, with a focus on molecular and cell biological research. Since the aim of this Special issue is to illustrate, through selected works, frontier research in osteoclasts, we encourage relevant experts and colleagues to contribute papers reflecting the latest progress in their particular research field. Even papers describing signal pathways alone and membrane trafficking alone are welcomed.

Prof. Takayuki Tsukuba
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

Topics include, without being limited to:

  • Osteoclast differentiation
  • Cell signaling
  • Membrane trafficking
  • Lysosomes
  • Podosomes
  • Receptors
  • Ion channels
  • Membrane proteins
  • Actin-binding proteins
  • Bone diseases

Published Papers (1 paper)

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Research

19 pages, 4851 KiB  
Article
Rab11A Functions as a Negative Regulator of Osteoclastogenesis through Dictating Lysosome-Induced Proteolysis of c-fms and RANK Surface Receptors
by Yuka Okusha, Manh Tien Tran, Mami Itagaki, Chiharu Sogawa, Takanori Eguchi, Tatsuo Okui, Tomoko Kadowaki, Eiko Sakai, Takayuki Tsukuba and Kuniaki Okamoto
Cells 2020, 9(11), 2384; https://doi.org/10.3390/cells9112384 - 31 Oct 2020
Cited by 13 | Viewed by 4541
Abstract
Osteoclast differentiation and activity are controlled by two essential cytokines, macrophage colony-stimulating factor (M-CSF) and the receptor activator of nuclear factor-κB ligand (RANKL). Rab11A GTPase, belonging to Rab11 subfamily representing the largest branch of Ras superfamily of small GTPases, has been identified as [...] Read more.
Osteoclast differentiation and activity are controlled by two essential cytokines, macrophage colony-stimulating factor (M-CSF) and the receptor activator of nuclear factor-κB ligand (RANKL). Rab11A GTPase, belonging to Rab11 subfamily representing the largest branch of Ras superfamily of small GTPases, has been identified as one of the crucial regulators of cell surface receptor recycling. Nevertheless, the regulatory role of Rab11A in osteoclast differentiation has been completely unknown. In this study, we found that Rab11A was strongly upregulated at a late stage of osteoclast differentiation derived from bone marrow-derived macrophages (BMMs) or RAW-D murine osteoclast precursor cells. Rab11A silencing promoted osteoclast formation and significantly increased the surface levels of c-fms and receptor activator of nuclear factor-κB (RANK) while its overexpression attenuated osteoclast formation and the surface levels of c-fms and RANK. Using immunocytochemical staining for tracking Rab11A vesicular localization, we observed that Rab11A was localized in early and late endosomes, but not lysosomes. Intriguingly, Rab11A overexpression caused the enhancement of fluorescent intensity and size-based enlargement of early endosomes. Besides, Rab11A overexpression promoted lysosomal activity via elevating the endogenous levels of a specific lysosomal protein, LAMP1, and two key lysosomal enzymes, cathepsins B and D in osteoclasts. More importantly, inhibition of the lysosomal activity by chloroquine, we found that the endogenous levels of c-fms and RANK proteins were enhanced in osteoclasts. From these observations, we suggest a novel function of Rab11A as a negative regulator of osteoclastogenesis mainly through (i) abolishing the surface abundance of c-fms and RANK receptors, and (ii) upregulating lysosomal activity, subsequently augmenting the degradation of c-fms and RANK receptors, probably via the axis of early endosomes–late endosomes–lysosomes in osteoclasts. Full article
(This article belongs to the Special Issue Signaling Pathways and Membrane Trafficking in Osteoclasts)
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