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Mechanical unloading triggers glutamine influx and catabolism to suppress osteoclast apoptosis

ABSTRACT: External mechanical stimuli are pivotal for the maintenance of bone homeostasis via enhancing bone formation and inhibiting bone resorption. Lack of mechanical loading during prolonged bed rest or exposure to long-term microgravity environment in space leads to a rapid decline in bone mass and bone strength. Osteoblast lineage cells are capable of sensing and transmitting mechanical signals through a variety of pathways. However, the mechanisms by which osteoclasts perceive and respond to mechanical disturbances remain largely unclear. Here, through integrating the data of single-cell transcriptome, metabolome, proteome and ubiquitinome of bone tissues from hindlimb unloading (HLU) and control mice, we clarify that in the absence of mechanical force, osteoclasts are characterized by significant increase in Gln influx and catabolism, as well as suppression of intrinsic apoptosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE263705 | GEO | 2025/09/09

REPOSITORIES: GEO

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Project description:Proctor2016 - Circadian rhythm of PTH and the dynamics of signaling molecules on bone remodeling This model is described in the article: Simulated Interventions to Ameliorate Age-Related Bone Loss Indicate the Importance of Timing. Proctor CJ, Gartland A. Front Endocrinol (Lausanne) 2016; 7: 61 Abstract: Bone remodeling is the continuous process of bone resorption by osteoclasts and bone formation by osteoblasts, in order to maintain homeostasis. The activity of osteoclasts and osteoblasts is regulated by a network of signaling pathways, including Wnt, parathyroid hormone (PTH), RANK ligand/osteoprotegrin, and TGF-?, in response to stimuli, such as mechanical loading. During aging there is a gradual loss of bone mass due to dysregulation of signaling pathways. This may be due to a decline in physical activity with age and/or changes in hormones and other signaling molecules. In particular, hormones, such as PTH, have a circadian rhythm, which may be disrupted in aging. Due to the complexity of the molecular and cellular networks involved in bone remodeling, several mathematical models have been proposed to aid understanding of the processes involved. However, to date, there are no models, which explicitly consider the effects of mechanical loading, the circadian rhythm of PTH, and the dynamics of signaling molecules on bone remodeling. Therefore, we have constructed a network model of the system using a modular approach, which will allow further modifications as required in future research. The model was used to simulate the effects of mechanical loading and also the effects of different interventions, such as continuous or intermittent administration of PTH. Our model predicts that the absence of regular mechanical loading and/or an impaired PTH circadian rhythm leads to a gradual decrease in bone mass over time, which can be restored by simulated interventions and that the effectiveness of some interventions may depend on their timing. This model is hosted on BioModels Database and identified by: BIOMD0000000612. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Mechanical unloading triggers glutamine influx and catabolism to suppress osteoclast apoptosis

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