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Bone Biology: A Molecular Perspective
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Bone Biology: A Molecular Perspective

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 March 2023) | Viewed by 4341

Special Issue Editor

Dr. Harish K. Datta

E-Mail Website
Guest Editor
Blood Sciences, South Tees Hospitals NHS Foundation Trust, Middlesbrough TS4 3BW, UK
Interests: osteoporosis; bone cells; molecular; cell signalling; therapies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Bone turnover, which involves resorption followed by replacement by new bone, is a lifelong process. This complex process involves inter- and intracellular signalling between the osteoprogenitor cells and differentiated bone to regulate bone remodelling and growth. Several advances in bone cell molecular biology have provided insight into various skeletal pathologies, providing opportunities for novel therapeutic targets. This Special Issue will cover emerging areas of bone epigenetic regulation by DNA methylation, non-coding RNAs and histone modification and multiple omics including transcriptomes, metabolomics and proteomics. The application of these technologies has led to the identification of macular factors and network, contributing to the pathogenesis of osteoporosis and other metabolic bone diseases.

Dr. Harish K. Datta
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. 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

  • bone
  • osteoporosis
  • metabolic bone disease
  • osteoclast
  • osteoblast
  • osteocytes
  • omics

Published Papers (2 papers)

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Research

19 pages, 9689 KiB  
Article
Osteocyte-Derived CaMKK2 Regulates Osteoclasts and Bone Mass in a Sex-Dependent Manner through Secreted Calpastatin
by Justin N. Williams, Mavis Irwin, Yong Li, Anuradha Valiya Kambrath, Brett T. Mattingly, Sheel Patel, Mizuho Kittaka, Rebecca N. Collins, Nicholas A. Clough, Emma H. Doud, Amber L. Mosley, Teresita Bellido, Angela Bruzzaniti, Lilian I. Plotkin, Jonathan C. Trinidad, William R. Thompson, Lynda F. Bonewald and Uma Sankar
Int. J. Mol. Sci. 2023, 24(5), 4718; https://doi.org/10.3390/ijms24054718 - 1 Mar 2023
Cited by 3 | Viewed by 2499
Abstract
Calcium/calmodulin (CaM)-dependent protein kinase kinase 2 (CaMKK2) regulates bone remodeling through its effects on osteoblasts and osteoclasts. However, its role in osteocytes, the most abundant bone cell type and the master regulator of bone remodeling, remains unknown. Here we report that the conditional [...] Read more.
Calcium/calmodulin (CaM)-dependent protein kinase kinase 2 (CaMKK2) regulates bone remodeling through its effects on osteoblasts and osteoclasts. However, its role in osteocytes, the most abundant bone cell type and the master regulator of bone remodeling, remains unknown. Here we report that the conditional deletion of CaMKK2 from osteocytes using Dentine matrix protein 1 (Dmp1)-8kb-Cre mice led to enhanced bone mass only in female mice owing to a suppression of osteoclasts. Conditioned media isolated from female CaMKK2-deficient osteocytes inhibited osteoclast formation and function in in vitro assays, indicating a role for osteocyte-secreted factors. Proteomics analysis revealed significantly higher levels of extracellular calpastatin, a specific inhibitor of calcium-dependent cysteine proteases calpains, in female CaMKK2 null osteocyte conditioned media, compared to media from female control osteocytes. Further, exogenously added non-cell permeable recombinant calpastatin domain I elicited a marked, dose-dependent inhibition of female wild-type osteoclasts and depletion of calpastatin from female CaMKK2-deficient osteocyte conditioned media reversed the inhibition of matrix resorption by osteoclasts. Our findings reveal a novel role for extracellular calpastatin in regulating female osteoclast function and unravel a novel CaMKK2-mediated paracrine mechanism of osteoclast regulation by female osteocytes. Full article
(This article belongs to the Special Issue Bone Biology: A Molecular Perspective)
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16 pages, 6921 KiB  
Article
Crucial Role of Lysine-Specific Histone Demethylase 1 in RANKL-Mediated Osteoclast Differentiation
by Mina Ding, Zhihao Chen, Eunjin Cho, Sang-Wook Park and Tae-Hoon Lee
Int. J. Mol. Sci. 2023, 24(4), 3605; https://doi.org/10.3390/ijms24043605 - 10 Feb 2023
Cited by 4 | Viewed by 1554
Abstract
Epigenetic regulators are involved in osteoclast differentiation. This study proposes that the inhibitors of epigenetic regulators could be effective in the treatment of osteoporosis. This study identified GSK2879552, a lysine-specific histone demethylase 1 (LSD1) inhibitor, as a candidate for the treatment of osteoporosis [...] Read more.
Epigenetic regulators are involved in osteoclast differentiation. This study proposes that the inhibitors of epigenetic regulators could be effective in the treatment of osteoporosis. This study identified GSK2879552, a lysine-specific histone demethylase 1 (LSD1) inhibitor, as a candidate for the treatment of osteoporosis from epigenetic modulator inhibitors. We investigate the function of LSD1 during RANKL-induced osteoclast formation. LSD1 small-molecule inhibitors effectively inhibit the RANKL-induced osteoclast differentiation in a dose-dependent manner. LSD1 gene knockout in macrophage cell line Raw 264.7 also inhibits RANKL-mediated osteoclastogenesis. LSD1-inhibitor-treated primary macrophage cells and LSD1 gene knockout Raw 264.7 cells failed to show actin ring formation. LSD1 inhibitors prevent the expression of RANKL-induced osteoclast-specific genes. They also downregulated the protein expression of osteoclast-related markers in osteoclastogeneses, such as Cathepsin K, c-Src, and NFATc1. Although LSD1 inhibitors were shown to reduce the in vitro demethylation activity of LSD1, they did not modulate the methylation of Histone 3 K4 and K9 during osteoclastogenesis. The ovariectomy (OVX)-induced osteoporosis model revealed that GSK2879552 slightly restores OVX-induced cortical bone loss. LSD1 can be employed as a positive regulator to promote osteoclast formation. Hence, inhibition of LSD1 activities is a potential target for preventing bone diseases characterized by excessive osteoclast activities. Full article
(This article belongs to the Special Issue Bone Biology: A Molecular Perspective)
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