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Biology
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Molecular Basis of Bone Homeostasis and Skeletal Diseases
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Molecular Basis of Bone Homeostasis and Skeletal Diseases

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

Deadline for manuscript submissions: 30 November 2024 | Viewed by 2000

Special Issue Editor

Dr. Weirong Xing

E-Mail Website
Guest Editor
1. Musculoskeletal Disease Center, Jerry L Pettis VA Medical Center, Loma Linda, CA 92357, USA
2. Department of Medicine, Loma Linda University, Loma Linda, CA 92354, USA
Interests: bone formation; bone resorption; osteoclast; osteoblast; osteoclast differentiation; osteoclast dysfunction; osteoblast differentiation; osteoblast activity; osteoprogenitor; coupling factor; osteoporosis; bone homeostasis; soluble factor; extracellular vesicle; lysosome; exocytosis; hormone; signal pathways; anti-resorption; small molecular inhibitor

Special Issue Information

Dear Colleagues,

Bone homeostasis involves both processes of osteoclast-mediated bone resorption and osteoblast-mediated bone formation. In physiological conditions, bone resorption is coupled with bone formation to maintain bone homeostasis. The destruction of bone tissue by active osteoclasts facilitates growth factor release from resorbed bone matrices, resulting in increased osteoblast proliferation as well as differentiation and bone formation. There are several regulatory factors that mediate osteoclast and osteoblast differentiation and activity. The deficiency or mutation of those factors could cause osteopetrosis or osteoporosis. Recently, there has been increasing interest in the identification of novel gene mutations associated with skeletal diseases and small molecular inhibitors that regulate osteoclast and osteoblast function, and the generation of new humanized mouse models. While significant advancements have been made, these relatively new fields of research are rapidly expanding. For this Special Issue, we invite researchers to contribute with either original research (both in vivo or in vitro studies) or review articles focusing on the molecular basis of bone homeostasis and skeletal diseases (in mice or in humans) in addition to the identification of new therapeutic agents that target osteoclast function or osteoblast activity.

Dr. Weirong Xing
Guest Editor

Manuscript Submission Information

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Keywords

  • osteoclast

  • osteoblast
  • bone
  • skeletal disease
  • bone formation
  • bone resorption
  • osteoporosis
  • osteopetrosis
  • human genetics
  • mouse genetics

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Published Papers (2 papers)

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Research

9 pages, 2382 KiB  
Communication
An In Vitro Orbital Flow Model to Study Mechanical Loading Effects on Osteoblasts
by Subburaman Mohan, Ritika Surisetty and Kesavan Chandrasekhar
Biology 2024, 13(9), 646; https://doi.org/10.3390/biology13090646 - 23 Aug 2024
Viewed by 478
Abstract
Flow induced by an orbital shaker is known to produce shear stress and oscillatory flow, but the utility of this model for studying mechanical loading effects in osteoblasts is not well defined. To test this, osteoblasts derived from the long bones of adult [...] Read more.
Flow induced by an orbital shaker is known to produce shear stress and oscillatory flow, but the utility of this model for studying mechanical loading effects in osteoblasts is not well defined. To test this, osteoblasts derived from the long bones of adult male C57BL/6J mice were plated on 6-well plates and subjected to orbital shaking at various frequencies (0.7, 1.4, and 3.3 Hz) for 30 and 60 min in serum-free differentiation media. The shear stress on cells produced by 0.7, 1.4, and 3.3 Hz shaking frequencies were 1.6, 4.5, and 11.8 dynes/cm2, respectively. ALP activity measured 72 h after shaking (orbital flow) showed a significant increase at 0.7 and 1.4 Hz, but not at 3.3 Hz, compared to static controls. Orbital flow-induced mechanical stress also significantly increased (25%) osteoblast proliferation at a 0.7 Hz flow compared to static controls. Additionally, expression levels of bone formation markers Osf2, Hif1a, Vegf, and Cox2 were significantly increased (1.5- to 3-fold, p < 0.05) in cells subjected to a 0.7 Hz flow compared to non-loaded control cells. We also evaluated the effect of orbital flow on key signaling pathways (mTOR, JNK, and WNT) known to mediate mechanical strain effects on osteoblasts. We found that blocking mTOR and WNT signaling with inhibitors significantly reduced (20–30%) orbital flow-induced ALP activity compared to cells treated using a vehicle. In contrast, inhibition of JNK signaling did not affect flow-induced osteoblast differentiation. In conclusion, our findings show that the flow produced by an orbital shaker at a lower frequency is an appropriate inexpensive model for studying the molecular pathways mediating mechanical strain effects on primary cultures of osteoblasts in vitro. Full article
(This article belongs to the Special Issue Molecular Basis of Bone Homeostasis and Skeletal Diseases)
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12 pages, 1818 KiB  
Article
Global and Conditional Disruption of the Igf-I Gene in Osteoblasts and/or Chondrocytes Unveils Epiphyseal and Metaphyseal Bone-Specific Effects of IGF-I in Bone
by Weirong Xing, Chandrasekhar Kesavan, Sheila Pourteymoor and Subburaman Mohan
Biology 2023, 12(9), 1228; https://doi.org/10.3390/biology12091228 - 12 Sep 2023
Cited by 1 | Viewed by 1117
Abstract
To evaluate the relative importance of IGF-I expression in various cell types for endochondral ossification, we quantified the trabecular bone at the secondary spongiosa and epiphysis of the distal femur in 8–12-week-old male mice with a global knockout of the Igf-I gene, as [...] Read more.
To evaluate the relative importance of IGF-I expression in various cell types for endochondral ossification, we quantified the trabecular bone at the secondary spongiosa and epiphysis of the distal femur in 8–12-week-old male mice with a global knockout of the Igf-I gene, as well as the conditional deletion of Igf-I in osteoblasts, chondrocytes, and osteoblasts/chondrocytes and their corresponding wild-type control littermates. The osteoblast-, chondrocyte-, and osteoblast/chondrocyte-specific Igf-I conditional knockout mice were generated by crossing Igf-I floxed mice with Cre transgenic mice in which Cre expression is under the control of either the Col1α2 or Col2α1 promoter. We found that the global disruption of Igf-I resulted in 80% and 70% reductions in bone size, defined as total volume, at the secondary spongiosa and epiphysis of the distal femur, respectively. The abrogation of Igf-I in Col1α2-producing osteoblasts but not Col2α1-producing chondrocytes decreased bone size by 25% at both the secondary spongiosa and epiphysis. In comparison, the deletion of the Igf-I globally or specifically in osteoblasts or chondrocytes reduced trabecular bone mass by 25%. In contrast, the universal deletion of Igf-I in all cells, but not the conditional disruption of Igf-I in osteoblasts and/or chondrocytes reduced trabecular bone mass in the epiphysis. The reduced trabecular bone mass at the secondary spongiosa in osteoblast- and/or chondrocyte-specific Igf-I conditional knockout mice is caused by the reduced trabecular number and increased trabecular separation. Immunohistochemistry studies found that the expression levels of chondrocyte (COL10, MMP13) and osteoblast (BSP) markers were less in the secondary spongiosa and the epiphyses in the global Igf-I deletion mice. Our data indicate that local and endocrine Igf-I act pleiotropically and in a cell type- and bone compartment-dependent manner in bone. Full article
(This article belongs to the Special Issue Molecular Basis of Bone Homeostasis and Skeletal Diseases)
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