Beta-1 Adrenergic Agonist Treatment Mitigates Negative Changes in Cancellous Bone Microarchitecture and Inhibits Osteocyte Apoptosis during Disuse

Swift, Joshua M.; Swift, Sibyl N.; Allen, Matthew R.; Bloomfield, Susan A.

doi:10.1371/journal.pone.0106904

Cited by 24 publications

(24 citation statements)

References 34 publications

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“…The increase in alveolar bone tissue mass upon atenolol treatment in this study is consistent with the decreased risk of fracture upon atenolol treatment reported previously (Song et al, ; Toulis et al, ) but not with an atenolol‐induced decrease in bone mass owing to systemic stimuli that promotes IGF‐1 downregulation reported previously (Pierroz et al, ). This discrepancy may result from differences in mechanical stress, orthodontic force and the dynamic cyclic axial compression protocol.…”

Section: Discussionsupporting

confidence: 93%

“…In contrast, Pierroz et al () reported a reduction in bone volume in β1‐AR‐knockout mice, while other studies reported an improvement in bone fragility by blocking β1‐AR (Song et al, ; Toulis, Hemming, Stergianos, Nirantharakumar, & Bilezikian, ). Furthermore, β1‐AR signalling is reported to present an anabolic stimulus in response to mechanical stimulation (Pierroz et al, ).…”

Section: Introductionmentioning

confidence: 92%

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Suppression of tooth movement‐induced sclerostin expression using β‐adrenergic receptor blockers

et al. 2020

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Objective Regulation of bone metabolism by the sympathetic nervous system has recently been clarified. Tooth movement is increased by increased bone metabolic turnover due to sympathetic activation. This study aimed to compare the effects of the β‐adrenergic receptor (β‐AR) blockers atenolol (β1‐AR blocker), butoxamine (β2‐AR blocker) and propranolol (non‐selective β‐AR blocker) on tooth movement in spontaneously hypertensive rats (SHR) with sympathicotonia. Materials and Methods Spontaneously hypertensive rats were divided into the following four groups: an SHR control group and groups treated with 0.1 mg/kg atenolol, 1 mg/kg butoxamine or 1 mg/kg propranolol (n = 6 rats/group). Atenolol, butoxamine or propranolol was administered daily to each treatment group, and orthodontic force was applied using a closed‐coil spring. Finally, immunohistochemical analysis was performed for receptor activator of nuclear factor kappa‐B ligand (RANKL) and sclerostin (SOST). Results Atenolol, butoxamine and propranolol inhibited tooth movement and increased maxillary alveolar bone volume. Histological analysis revealed that these β‐AR blockers decreased osteoclast activity on the compression side. Furthermore, immunohistochemical analysis revealed that atenolol, butoxamine and propranolol decreased the number of RANKL‐ and SOST‐positive osteocytes on the compression side. Conclusions β‐AR blockers decreased tooth movement and downregulated SOST in osteocytes, accompanied by increasing alveolar bone resorption.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 92%

Suppression of tooth movement‐induced sclerostin expression using β‐adrenergic receptor blockers

et al. 2020

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“…ADRB1 plays a critical protective role in hypoxia/reoxygenation-induced neonatal rat cardiomyocyte injury in vitro [ 47 ]. Swift et al indicated that ADRB1 agonist treatment during dobutamine disuse mitigates negative changes in cancellous bone microarchitecture and inhibits increases in osteocyte apoptosis [ 48 ]. In addition, Zapater et al proposed that Beta-adrenergic receptor-1 antagonist accelerates liver norepinephrine modulation of the pro-inflammatory response in CCl(4)-treated mice [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal stem cell conditioned medium alleviates oxidative stress injury induced by hydrogen peroxide via regulating miR143 and its target protein in hepatocytes

et al. 2017

BMC Immunol

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BackgroundTo investigate the impact of miRNA (microRNA) on hepatic oxidative stress damage under the human mesenchymal stem cell conditioned medium (MSC-CM) and explore the roles of the beta-1 adrenergic receptor (ADRB1) and hexokinase 2 (HK2) in this process.MethodsHydrogen peroxide was used to induce oxidative stress injury in the human normal liver cell line L02. MSC-CM was separately prepared. After treatment with MSC-CM, the protective effects of MSC-CM on oxidative stress injury were assessed by changes in apoptosis, cell viability, cell cycle, and mitochondrial membrane potential. According to the microarray analysis, 19 disparately expressed miRNAs were selected for RT-PCR and miR143 identified as having significant differential expression in MSC-CM against oxidative stress injury. Subsequently, the predicted target proteins of miR143 were selected by bioinformatics software, and verified by western blot. In addition, down-regulation and up-regulation of miR143 expression and hydrogen peroxide induced hypoxia injury were carried out on L02 cells to study the role of miR143.ResultsMSC-CM significantly attenuated H2O2 induced oxidative stress injury. The expression of miR143 was increased following oxidative stress injury whereas it decreased after MSC-CM treatment. The expression levels of HK2 and ADRB1 regulated by miR143 and Bcl-2 decreased under H2O2 treatment but were restored following MSC-CM treatment. However the expression levels of Bax and BMF increased after H2O2 injury and decreased after MSC-CM treatment. Moreover over-expression or down-regulation of miR143 aggravated or alleviated hepatocyte apoptosis respectively.ConclusionsMSC-CM may alleviate H2O2 induced oxidative stress injury by inhibiting apoptosis and adjusting miRNA expression. Moreover down-regulation of miR143 protects L02 cells from apoptosis and initiates an adaptive process by adjusting the expression of HK2 ADRB1 and apoptosis-related proteins.Electronic supplementary materialThe online version of this article (10.1186/s12865-017-0232-x) contains supplementary material, which is available to authorized users.

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“…Similarly, others found that treatment of rats with propranolol or a leptin analog during 28 days of hindlimb unloading reduced unloading-associated bone loss; propranolol treatment effectively preserved bone formation and prevented increased bone resorption, while leptin analog treatment was only able to prevent changes in osteoclastic bone resorption ( 101 ). Conversely, treatment of rats with a β1-adrenergic receptor agonist (dobutamine) attenuated hindlimb unloading-induced bone loss, prevented the decline in bone formation induced by unloading, and diminished unloading-induced osteocyte apoptosis ( 102 , 103 ).…”

Section: Nerves and Skeletal Adaptationmentioning

confidence: 99%

The Role of Nerves in Skeletal Development, Adaptation, and Aging

et al. 2020

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The skeleton is well-innervated, but only recently have the functions of this complex network in bone started to become known. Although our knowledge of skeletal sensory and sympathetic innervation is incomplete, including the specific locations and subtypes of nerves in bone, we are now able to reconcile early studies utilizing denervation models with recent work dissecting the molecular signaling between bone and nerve. In total, sensory innervation functions in bone much as it does elsewhere in the body—to sense and respond to stimuli, including mechanical loading. Similarly, sympathetic nerves regulate autonomic functions related to bone, including homeostatic remodeling and vascular tone. However, more study is required to translate our current knowledge of bone-nerve crosstalk to novel therapeutic strategies that can be effectively utilized to combat skeletal diseases, disorders of low bone mass, and age-related decreases in bone quality.

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Beta-1 Adrenergic Agonist Treatment Mitigates Negative Changes in Cancellous Bone Microarchitecture and Inhibits Osteocyte Apoptosis during Disuse

Cited by 24 publications

References 34 publications

Suppression of tooth movement‐induced sclerostin expression using β‐adrenergic receptor blockers

Suppression of tooth movement‐induced sclerostin expression using β‐adrenergic receptor blockers

Mesenchymal stem cell conditioned medium alleviates oxidative stress injury induced by hydrogen peroxide via regulating miR143 and its target protein in hepatocytes

The Role of Nerves in Skeletal Development, Adaptation, and Aging

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