Circadian Regulation of Bone

Maria, Sifat; Witt‐Enderby, Paula A.

doi:10.1007/978-3-319-64543-8_3

Cited by 4 publications

(6 citation statements)

References 76 publications

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“…Similarly, individuals with Smith‐Magenis syndrome have abnormal melatonin secretion rhythms and disturbed skeletal development 120,121 . LAN also reduces Per2 expression and elevates cortisol levels to modify the diurnal rhythms of bone metabolism in rodents 122 . This finding corroborates Ostrowska et al.…”

Section: Factors Affecting the Bone Circadian Clocksupporting

confidence: 64%

The specificities, influencing factors, and medical implications of bone circadian rhythms

Mei,

Wang,

Wang

et al. 2024

The FASEB Journal

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Physiological processes within the human body are regulated in approximately 24‐h cycles known as circadian rhythms, serving to adapt to environmental changes. Bone rhythms play pivotal roles in bone development, metabolism, mineralization, and remodeling processes. Bone rhythms exhibit cell specificity, and different cells in bone display various expressions of clock genes. Multiple environmental factors, including light, feeding, exercise, and temperature, affect bone diurnal rhythms through the sympathetic nervous system and various hormones. Disruptions in bone diurnal rhythms contribute to the onset of skeletal disorders such as osteoporosis, osteoarthritis and skeletal hypoplasia. Conversely, these bone diseases can be effectively treated when aimed at the circadian clock in bone cells, including the rhythmic expressions of clock genes and drug targets. In this review, we describe the unique circadian rhythms in physiological activities of various bone cells. Then we summarize the factors synchronizing the diurnal rhythms of bone with the underlying mechanisms. Based on the review, we aim to build an overall understanding of the diurnal rhythms in bone and summarize the new preventive and therapeutic strategies for bone disorders.

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Section: Factors Affecting the Bone Circadian Clocksupporting

confidence: 64%

The specificities, influencing factors, and medical implications of bone circadian rhythms

Mei,

Wang,

Wang

et al. 2024

The FASEB Journal

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“…Significant relationships between depression, bone mineral density, and cortisol levels have been reported where depressed patients were shown to have higher cortisol levels and lower bone mineral density compared to placebo controls . Also, lifestyle that includes sleep disruption through shift work, sleep deprivation, physical strength, weight gain, and stress levels can adversely affect bone. Besides improving compliance, the positive effect of melatonin on mood and sleep may show benefits to bone by reducing cortisol levels and re‐entraining sleep/wake cycles to coincide with the light/dark cycle and natural bone rhythms.…”

Section: Discussionmentioning

confidence: 99%

“…Significant relationships between depression, bone mineral density, and cortisol levels have been reported, and so any improvement in any of these variables could also contribute to melatonin's beneficial effects on bone. Therefore, the daily diary logs kept by the MOPS cohort were further analyzed to provide additional data to explain melatonin's beneficial actions (eg, lifestyle, mood, sleep) on bone as described in other studies …”

Section: Introductionmentioning

confidence: 99%

Biological effects of melatonin on osteoblast/osteoclast cocultures, bone, and quality of life: Implications of a role for MT2 melatonin receptors, MEK1/2, and MEK5 in melatonin‐mediated osteoblastogenesis

Maria

Samsonraj

Munmun

et al. 2018

Journal of Pineal Research

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132

164

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The Melatonin Osteoporosis Prevention Study (MOPS) demonstrated that nightly melatonin resulted in a time-dependent decrease in equilibrium ratios of serum osteoclasts and osteoblasts in perimenopausal women. This study examines mechanisms related to the ratios of osteoblasts and osteoclasts using coculture models (transwell or layered) of human mesenchymal stem cell (MSC) and human peripheral blood monocytes (PBMCs). Human MSC/PBMC cocultures exposed to melatonin in osteogenic (OS+) medium for 21 days induced osteoblast differentiation and mineralization; however, only in layered cocultures did melatonin inhibit osteoclastogenesis. Melatonin effects were mediated through MT2 melatonin receptors, MEK1/2, and MEK5. In layered but not transwell cocultures, melatonin increased OPG:RANKL ratios by inhibiting RANKL, suggesting that contact with osteoclasts during osteoblastogenesis inhibits RANKL secretion. Melatonin modulated expression of ERK1/2, ERK5, β1 integrin, GLUT4, and IRβ that was dependent upon the type of coculture; however, in both cultures, melatonin increased RUNX2 and decreased PPARγ expression, indicating a role for metabolic processes that control osteogenic vs adipogenic cell fates of MSCs. Furthermore, melatonin also has osteoblast-inducing effects on human adipose-derived MSCs. In vivo, one-year nightly melatonin (15 mg/L) given to neu female mice in their drinking water increased pErk1/2, pErk5, Runx2, and Opg and Rankl levels in bone consistent with melatonin's already reported bone-enhancing effects. Finally, analysis of daily logs from the MOPS demonstrated a significant improvement in mood and perhaps sleep quality in women receiving melatonin vs placebo. The osteoblast-inducing, bone-enhancing effects of melatonin and improvement in quality of life suggest that melatonin is a safe and effective bone loss therapy.

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“…Employing a lentiviral vector containing RNAi series, Zhuo et al [ 21 ] reduced Bmal1 transcription in bone marrow-derived MSCs (BMSCs), increasing the osteogenic differentiation potential of BMSCs. Maria and Witt-Enderby [ 22 ] characterized clock gene expressions and functions in bone, as well as how its rhythm affects osteoblasts and osteoclasts' activities and differentiation, as well as bone metabolism; they further addressed factors, which cause circadian interruption of bone rhythms, as well as methods of managing healthier bones in a society that improves it. Li et al [ 23 ] identified and demonstrated the involvement of cholesterol-25-hydroxylase (CH25H) in stem cell development, as well as investigated the process.…”

Section: Related Workmentioning

confidence: 99%

Meta-Analysis of Mechanism of Influence of CRY2 on the Differentiation of Mouse Osteoblast through the Regulation of Wnt/Β-Catenin Signaling Pathway

Yang

Xie

et al. 2022

BioMed Research International

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Noncoding RNAs were discovered to control a variety of developmental mechanisms, including osteogenesis. According to emerging evidence, cryptochrome circadian-regulating (CRY) proteins have emerged as essential controllers of osteoblast differentiation. The linked processes, on the other hand, are still unknown. The specific process that underpins osteoblast differentiation and proliferation is yet unknown. This research gives a meta-analysis of CRY2’s impact on mouse osteoblast differentiation via the control of the WNT/β–catenin signaling pathways. Western blot and quantitative real-time PCR were used to identify Cry2 expression levels, components in the osteoblast-associated signaling pathway, and osteoblast transcription markers. The osteogenic condition was measured utilizing alkaline phosphatase (ALP) and alizarin red (AR) staining, whereas cell growth rates were measured using CCK8 assays. An ectopic bone formation experiment was used to determine the osteogenic potential of osteoblasts. Cry2 stimulates the osteogenic development of mouse osteoblasts through canonical Wnt/β-catenin signaling, according to the findings.

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Circadian Regulation of Bone

Cited by 4 publications

References 76 publications

The specificities, influencing factors, and medical implications of bone circadian rhythms

The specificities, influencing factors, and medical implications of bone circadian rhythms

Biological effects of melatonin on osteoblast/osteoclast cocultures, bone, and quality of life: Implications of a role for MT2 melatonin receptors, MEK1/2, and MEK5 in melatonin‐mediated osteoblastogenesis

Meta-Analysis of Mechanism of Influence of CRY2 on the Differentiation of Mouse Osteoblast through the Regulation of Wnt/Β-Catenin Signaling Pathway

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