Bone Cell Biology

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1286

Special Issue Editors


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Guest Editor
Department of Cellular and Molecular Medicine, University of California, San Diego, CA 92093, USA
Interests: cellular and molecular medicine; bone; osteoclast; osteoblast; osteocyte; inflammation

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Guest Editor
1. Department of Clinical and Experimental Medicine, Endocrinology Unit I-II, University of Pisa and University Hospital of Pisa, Via Paradisa 2, 56124 Pisa, Italy
2. Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Interests: Graves’ disease; hyperthyroidism; GD extrathyroidal manifestations; thyroid autoimmunity; thyroid disease; Graves’ orbitopathy
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Special Issue Information

Dear Colleagues,

Bone remodeling is directly coordinated by three skeletal cell types: osteoclasts, osteoblasts and osteocytes for the removal of old bone and formation of new bone. As bone remodeling is a complex and delicate process mediated by all skeletal cells, the disfunction of cell–cell communications can lead to an imbalance and related diseases. Therapeutic approaches for bone diseases predominantly relieve symptoms and improve bone structural features, while there has not been an established therapy to realize longer-acting bone mass and density maintenance while decreasing the side effects. The current challenge is to understand the functional interactions between molecular networks underying cell–cell communications integrated by cell signaling, and also how the genomic architecture is changed in health and disease. This journal publishes the outstanding progress and novel understanding relating bone biology. The journal highlights breakthrough discoveries in basic studies related to bone physiology and pathology. Submissions are favored regarding basic studies on bone development and metabolism in its related diseases. In particular, this Special Issue focuses on mechanistic studies showing multi-omics data integration including epigenetics, transcriptomics and/or proteomics.

Dr. Yohei Abe
Dr. Giulia Lanzolla
Guest Editors

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Keywords

  • osteoclast
  • osteoblast
  • osteocyte
  • bone density
  • macrophage
  • RANK
  • transcription factor
  • cell signaling

Published Papers (1 paper)

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Research

12 pages, 1707 KiB  
Article
Targeted Overexpression of Claudin 11 in Osteoblasts Increases Trabecular Bone Mass by Stimulating Osteogenesis at the Expense of Adipogenesis in Mice
by Weirong Xing, Sheila Pourteymoor, Anakha Udayakumar, Yian Chen and Subburaman Mohan
Biology 2024, 13(2), 108; https://doi.org/10.3390/biology13020108 - 09 Feb 2024
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Abstract
Mice lacking Claudin11 (Cldn11) manifest reduced trabecular bone mass. However, the impact of Cldn11 expression in osteoblasts in vivo remains understudied. Herein, we generated osteoblast-specific transgenic (Tg) mice expressing Cldn11 and characterized their skeletal phenotype. Micro-CT analyses of the distal metaphysis [...] Read more.
Mice lacking Claudin11 (Cldn11) manifest reduced trabecular bone mass. However, the impact of Cldn11 expression in osteoblasts in vivo remains understudied. Herein, we generated osteoblast-specific transgenic (Tg) mice expressing Cldn11 and characterized their skeletal phenotype. Micro-CT analyses of the distal metaphysis of the femur showed a 50% and a 38% increase in trabecular bone mass in Tg male and female mice, respectively, due to a significant increase in trabecular number and a reduction in trabecular separation. Histomorphometry and serum biomarker studies uncovered that increased trabecular bone mass in Cldn11 Tg mice was the consequence of enhanced bone formation. Accordingly, an abundance of bone formation (Alp, Bsp), but not bone resorption (Ctsk), markers were augmented in the femurs of Cldn11 Tg mice. Since the trabecular bone density is known to inversely correlate with the amount of marrow adipose tissue (MAT), we measured the MAT in osmium-tetroxide-labeled bones by micro-CT scanning. We found 86% less MAT in the proximal tibia of the Tg males. Consistently, the expression levels of the adipogenic markers, adiponectin and leptin, were 50% lower in the femurs of the Tg males. Our data are consistent with the possibility that claudin11 exerts anabolic effects in osteoblastic lineage cells that act via promoting the differentiation of marrow stem cells towards osteoblasts at the expense of adipocytes. Full article
(This article belongs to the Special Issue Bone Cell Biology)
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