Special Issues

Transcription Factors in Bone: Developmental and Pathological Aspects
Editor: Jun Hirayama

Submission Deadline: 31 January 2024 (Status: Open)

Special Issue Editor

Dr. Jun Hirayama      Email   |   Website
Department of Clinical Engineering, Faculty of Health Sciences, Komatsu University, Komatsu, Ishikawa, Japan
Interests: body clock; biometrics; medical engineering; transcription; zebrafish

Special Issue Information

Dear Colleagues,

Bone tissue consists of osteoblasts, osteoclasts, osteocytes, and calcified bone matrices including hydroxyapatite, bone γ-carboxyglutamic acid protein, osteonectin, and type 1 collagen. The correct regulation and maintenance of the activities and structures of these components are required for bone homeostasis. A variety of signaling pathways, transcription factors, and chemical modifications of proteins are involved in the functional and structural regulation of bone components, such as activities, interactions, and differentiation of bone cells. Several pathophysiological conditions are known to induce impairments in the regulation of bone components, resulting in bone diseases. For example, reduced bone mineral density and diabetic vascular complications have been reported to increase the risk of fracture and osteoporosis in patients with type 1 diabetes. However, the mechanisms underlying pathophysiological condition-induced fracture and osteoporosis has not been fully understood.

A variety of endogenous systems are involved in the regulation of bone homeostasis. One example is the circadian clock, which generates biochemical and physiological rhythms with approximately 24 h periodicity. Previous studies have found a relation between the circadian clock and changes in bone functions and structure. In fact, several key transcriptional factors regulating the circadian clock play a role in bone metabolism. These findings support the hypothesis that the identification of novel transcriptional factors regulating the genes encoding bone components may contribute to understand the associations of bone homeostasis with other physiological regulatory mechanisms.

This research topic will focus on novel molecular and physiological mechanisms underlying the regulation of bone homeostasis. It aims to further understand the mechanisms for which impairments in this regulation are related to deficits in physiological processes that lead to disease and poor health. Submissions can feature current topical areas including, but not limited to the chronobiology of bone metabolism, food timing and exercise, osteoimmunology, melatonin, and biology of the gut microbiome.

Jun Hirayama
Guest Editor


body clock; biometrics; medical engineering; transcription; zebrafish

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  • Article
    Kouhei Kuroda, Ajai K. Srivastav, Akiko Suzuki, Muhammad Ahya Rafiuddin, Kenji Toyota, Masato Endo, Masato Honda, Kazuki Watanabe, Yusuke Maruyama, Yoshiaki Tabuchi, Atsuhiko Hattori, Makoto Urata, Hajime Matsubara, Nobuo Suzuki
    Journal of Biological Regulators and Homeostatic Agents. 2023, 37(10): 5141-5149. https://doi.org/10.23812/j.biol.regul.homeost.agents.20233710.498
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    Background: The corpuscles of Stannius (CS) are endocrine glands that regulate homeostasis of minerals, including calcium and phosphate, in bony fish. The hormone secreted by the CS, known as stanniocalcin, has been found in humans and bony fish. In mammals, stanniocalcin expressed in osteoblasts and has been reported to regulate osteoblastic differentiation. However, the details regarding its effect on osteoclasts remain uninvestigated. Therefore, in this study, we aimed to evaluate the effects of stanniocalcin on bone metabolism, including osteoclasts.

    Methods: Stanniocalcin is composed of approximately 250 amino acids, including several cysteines and glycans. Artificially synthesizing this hormone is difficult. In the present study, we used the CS extract to evaluate the effects of stanniocalcin on bone metabolism. Moreover, we established an in vitro bioassay system utilizing goldfish scales as a coexistence model of osteoblasts (bone-forming cells) and osteoclasts (bone-resorbing cells) in the calcified bone matrix. Using the goldfish scales, we examined the effects of CS extract treatment on the mRNA expressions of osteoclast- and osteoblast-related genes. Furthermore, to assess the inhibitory action of osteoclasts, we examined the receptor activator for NF-κB ligand (Rankl), osteoclastogenesis-promoting factor, osteoprotegerin (Opg), osteoclastogenesis inhibition factor, involved in the osteoblast–osteoclast interaction.

    Results: The expression of osteoblastic markers, such as alkaline phosphatase and collagen type I alpha 1 (Col1a1), significantly increased 6 h post-treatment with the CS extract. At 18 h post-incubation, Col1a1 and osteocalcin mRNA expressions in the treated scales also significantly upregulated. Conversely, at 6 and 18 h post-incubation, the mRNA expression of osteoclastic markers, cathepsin K, tartrate-resistant acid phosphatase, and matrix metalloproteinase-9, significantly decreased. Further, at 6 h post-incubation, Rankl/Opg expression significantly decreased on adding the CS extract.

    Conclusions: The CS extract was found to inhibit the osteoclastic activity by modulating Rankl/Opg expression. Thus, stanniocalcin inhibits the osteoclastic activity but promotes osteoblastic activity and bone formation.