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Article: [Control of bone remodeling by nervous system. Regulation of bone metabolism by peripheral nervous system].

Togari, Akifumi

2010 Volume 20, Issue 12, Page(s) 1831–1838

Abstract: Bone is richly innervated with adrenergic and peptidergic nerve terminals, and these play important roles in bone remodeling. Recent study confirmed a functional nerve-osteoblastic interplay by using an in vitro co-culture model comprising mouse ... ...

Abstract	Bone is richly innervated with adrenergic and peptidergic nerve terminals, and these play important roles in bone remodeling. Recent study confirmed a functional nerve-osteoblastic interplay by using an in vitro co-culture model comprising mouse osteoblastic cells and neurite-spouting mouse superior cervical ganglia. This indicates that nerve-osteoblastic cell cross-talk can occur for the dynamic regulation of local bone metabolism by peripheral nervous system. This review summarized both in vivo and in vitro evidences implicating peripheral neuron action in bone metabolism.
MeSH term(s)	Animals ; Bone Remodeling/physiology ; Bone and Bones/innervation ; Bone and Bones/metabolism ; Humans ; Mice ; Neurites/physiology ; Neurons/physiology ; Neurotransmitter Agents/physiology ; Norepinephrine/physiology ; Osteoblasts/physiology ; Osteoclasts/physiology ; Peripheral Nervous System/physiology ; Receptors, Adrenergic, beta-2/physiology ; Superior Cervical Ganglion/physiology ; Synapses
Chemical Substances	Neurotransmitter Agents ; Receptors, Adrenergic, beta-2 ; Norepinephrine (X4W3ENH1CV)
Language	Japanese
Publishing date	2010-12
Publishing country	Japan
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	2386417-5
ISSN	0917-5857
ISSN	0917-5857
DOI	CliCa101218311838
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Article ; Online: Systemic administration of low-dose naltrexone increases bone mass due to blockade of opioid growth factor receptor signaling in mice osteoblasts.

Tanaka, Kenjiro / Kondo, Hisataka / Hamamura, Kazunori / Togari, Akifumi

Life sciences

2019 Volume 224, Page(s) 232–240

Abstract: Aims: Opioid receptor blockers such as naloxone and naltrexone have been suggested to have a bone mass-increasing effect. However, the mechanisms at play have not been clarified. We examined the effects of naltrexone on osteoblasts and determined the ... ...

Abstract	Aims: Opioid receptor blockers such as naloxone and naltrexone have been suggested to have a bone mass-increasing effect. However, the mechanisms at play have not been clarified. We examined the effects of naltrexone on osteoblasts and determined the expression of opioid growth factor receptor (OGFR) in osteoblasts. Naltrexone blocks the OGFR and other canonical opioid receptors. Thus, we designed experiments to clarify the effects of naltrexone on bone tissue by examining the physiological role of OGFR signaling in osteoblasts and the changes in bone structure after naltrexone systemic administration in mice. Main methods: We used mouse osteoblast-like cell line MC3T3-E1 for in vitro experiments. We cultured MC3T3-E1 cells in the presence of the OGFR agonist met-enkephalin (met-enk). Then, we measured cell proliferation activity and analyzed the expression levels of cell proliferation-related genes. For our in vivo experiments, we administered naltrexone intraperitoneally to mice daily for 28 days and administered the animals in the control group equivalent volumes of saline. After sacrificing the mice, we performed micro-computed tomography and bone morphology analyses. Key findings: Met-enk suppressed cell proliferation in MC3T3-E1 cells. Moreover, Low dose naltrexone administration significantly increased their femoral bone mass, bone formation ratio, and osteoblast number/bone surface values when comparing the values for the same variables in the control group. Significance: Our results suggest that naltrexone increases bone mass due to osteoblast number increments caused by the OGFR signaling block. Opioid receptor blockers have potential as therapeutic agents for osteoporosis as well as opioid antagonists.
MeSH term(s)	Animals ; Bone Density/drug effects ; Cell Proliferation ; Cells, Cultured ; Enkephalin, Methionine/pharmacology ; Male ; Mice ; Mice, Inbred ICR ; Naltrexone/administration & dosage ; Naltrexone/pharmacology ; Narcotic Antagonists/administration & dosage ; Narcotic Antagonists/pharmacology ; Neurotransmitter Agents/pharmacology ; Osteoblasts/cytology ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Receptors, Opioid/chemistry ; Receptors, Opioid/genetics ; Receptors, Opioid/metabolism
Chemical Substances	Narcotic Antagonists ; Neurotransmitter Agents ; Receptors, Opioid ; methionine-enkephalin receptor ; Enkephalin, Methionine (58569-55-4) ; Naltrexone (5S6W795CQM)
Language	English
Publishing date	2019-03-28
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2019.03.069
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Article: [Increased bone resorption by sympathetic nervous activity].

Togari, Akifumi

Clinical calcium

2006 Volume 16, Issue 2, Page(s) 298–303

Abstract: Recent experimental studies showed the dynamic neural regulation of local bone metabolism. Increased sympathetic nervous activity has been demonstrated to cause bone loss via an increase in bone resorption and a decrease in bone formation. This review ... ...

Abstract	Recent experimental studies showed the dynamic neural regulation of local bone metabolism. Increased sympathetic nervous activity has been demonstrated to cause bone loss via an increase in bone resorption and a decrease in bone formation. This review summarized both in vivo and in vitro evidences implicating sympathetic neuron action in bone resorption.
MeSH term(s)	Animals ; Bone Resorption/physiopathology ; Osteoclasts/physiology ; Sympathetic Nervous System/physiology
Language	Japanese
Publishing date	2006-02
Publishing country	Japan
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	2386417-5
ISSN	0917-5857
ISSN	0917-5857
DOI	CliCa0602298303
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Article ; Online: Guanabenz inhibits alveolar bone resorption in a rat model of periodontitis.

Muramatsu, Ryujiro / Sato, Takuma / Hamamura, Kazunori / Miyazawa, Ken / Takeguchi, Atsushi / Tabuchi, Masako / Togari, Akifumi / Goto, Shigemi

Journal of pharmacological sciences

2021 Volume 147, Issue 3, Page(s) 294–304

Abstract: Increase of sympathetic activity has been known to exacerbate osteoporosis through promotion of bone resorption. However, it is largely unknown about involvement of sympathetic activity in exacerbation of periodontitis. In this study, we investigated ... ...

Abstract	Increase of sympathetic activity has been known to exacerbate osteoporosis through promotion of bone resorption. However, it is largely unknown about involvement of sympathetic activity in exacerbation of periodontitis. In this study, we investigated whether α
MeSH term(s)	Adrenergic alpha-2 Receptor Agonists/administration & dosage ; Adrenergic alpha-2 Receptor Agonists/pharmacology ; Animals ; Bone Resorption/etiology ; Bone Resorption/metabolism ; Bone Resorption/physiopathology ; Bone Resorption/prevention & control ; Cytokines/metabolism ; Disease Models, Animal ; Guanabenz/administration & dosage ; Guanabenz/pharmacology ; Inflammation Mediators/metabolism ; Male ; Periodontitis/complications ; Periodontitis/metabolism ; Periodontitis/physiopathology ; Periodontium/metabolism ; Rats, Inbred SHR ; Rats, Inbred WKY ; Sympathetic Nervous System/drug effects ; Sympathetic Nervous System/physiopathology ; Rats
Chemical Substances	Adrenergic alpha-2 Receptor Agonists ; Cytokines ; Inflammation Mediators ; Guanabenz (GGD30112WC)
Language	English
Publishing date	2021-08-14
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2021.08.003
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Article: Systemic administration of low-dose naltrexone increases bone mass due to blockade of opioid growth factor receptor signaling in mice osteoblasts

Tanaka, Kenjiro / Hamamura, Kazunori / Kondo, Hisataka / Togari, Akifumi

Life sciences. 2019 May 01, v. 224

2019

Abstract: Opioid receptor blockers such as naloxone and naltrexone have been suggested to have a bone mass-increasing effect. However, the mechanisms at play have not been clarified. We examined the effects of naltrexone on osteoblasts and determined the ... ...

Abstract	Opioid receptor blockers such as naloxone and naltrexone have been suggested to have a bone mass-increasing effect. However, the mechanisms at play have not been clarified. We examined the effects of naltrexone on osteoblasts and determined the expression of opioid growth factor receptor (OGFR) in osteoblasts. Naltrexone blocks the OGFR and other canonical opioid receptors. Thus, we designed experiments to clarify the effects of naltrexone on bone tissue by examining the physiological role of OGFR signaling in osteoblasts and the changes in bone structure after naltrexone systemic administration in mice.We used mouse osteoblast-like cell line MC3T3-E1 for in vitro experiments. We cultured MC3T3-E1 cells in the presence of the OGFR agonist met-enkephalin (met-enk). Then, we measured cell proliferation activity and analyzed the expression levels of cell proliferation-related genes. For our in vivo experiments, we administered naltrexone intraperitoneally to mice daily for 28 days and administered the animals in the control group equivalent volumes of saline. After sacrificing the mice, we performed micro-computed tomography and bone morphology analyses.Met-enk suppressed cell proliferation in MC3T3-E1 cells. Moreover, Low dose naltrexone administration significantly increased their femoral bone mass, bone formation ratio, and osteoblast number/bone surface values when comparing the values for the same variables in the control group.Our results suggest that naltrexone increases bone mass due to osteoblast number increments caused by the OGFR signaling block. Opioid receptor blockers have potential as therapeutic agents for osteoporosis as well as opioid antagonists.
Keywords	agonists ; bone density ; bone formation ; cell lines ; cell proliferation ; femur ; genes ; in vitro studies ; in vivo studies ; mice ; micro-computed tomography ; naloxone ; narcotic antagonists ; osteoblasts ; osteoporosis ; receptors ; therapeutics
Language	English
Dates of publication	2019-0501
Size	p. 232-240.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2019.03.069
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Article ; Online: Effects of a β2-adrenergic receptor blocker on experimental periodontitis in spontaneously hypertensive rats.

Takeguchi, Atsushi / Miyazawa, Ken / Sato, Takuma / Tabuchi, Masako / Muramatsu, Ryujiro / Maeda, Hatsuhiko / Togari, Akifumi / Goto, Shigemi

Life sciences

2021 Volume 277, Page(s) 119593

Abstract: Aims: Recent studies have reported a relationship between periodontal disease and hypertension, and previous evidence suggests that the sympathetic nervous system plays an important role in the control of bone metabolism. This study sought to evaluate ... ...

Abstract	Aims: Recent studies have reported a relationship between periodontal disease and hypertension, and previous evidence suggests that the sympathetic nervous system plays an important role in the control of bone metabolism. This study sought to evaluate the effect of the beta-2 adrenergic receptor (β2-AR) blocker butoxamine on experimental periodontitis in a rat model. Materials and methods: Wistar-Kyoto and spontaneously hypertensive rats (n = 6 per group) were orally administered butoxamine 1 mg/kg/day and experimental periodontitis was induced by applying an orthodontic ligature wire. The rats were sacrificed after 4 weeks and the residual alveolar bone was measured using micro-computed tomography (micro-CT) imaging analysis software for histological analysis. Key findings: Micro-CT imaging analysis showed a higher ratio of residual alveolar bone, BV/TV, and Tb.N in both Wistar-Kyoto and spontaneously hypertensive rats treated with butoxamine compared with the corresponding control rats. In histological analysis, compared with the Wistar-Kyoto and spontaneously hypertensive rat control groups, the corresponding butoxamine-treated groups showed a lower ratio of attachment level, lower values of osteoclast number and surface. Significance: β2-AR blockers maintained the alveolar bone mass and attachment level by suppressing osteoclast activity. Thus, β2-AR blockers may be effective in preventing periodontitis.
MeSH term(s)	Adrenergic beta-2 Receptor Antagonists/pharmacology ; Alveolar Bone Loss/metabolism ; Animals ; Blood Pressure/drug effects ; Bone Density/drug effects ; Bone and Bones/drug effects ; Butoxamine/metabolism ; Butoxamine/pharmacology ; Female ; Hypertension/metabolism ; Male ; Osteoclasts/drug effects ; Periodontitis/drug therapy ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptors, Adrenergic/metabolism ; Receptors, Adrenergic, beta-2/metabolism ; Sympathetic Nervous System/drug effects ; X-Ray Microtomography/methods
Chemical Substances	Adrenergic beta-2 Receptor Antagonists ; Receptors, Adrenergic ; Receptors, Adrenergic, beta-2 ; Butoxamine (0NM31M53PW)
Language	English
Publishing date	2021-05-09
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.119593
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Article ; Online: Attenuation of Bone Formation through a Decrease in Osteoblasts in Mutant Mice Lacking the GM2/GD2 Synthase Gene.

Sasaki, Eri / Hamamura, Kazunori / Mishima, Yoshitaka / Furukawa, Koichi / Nagao, Mayu / Kato, Hanami / Hamajima, Kosuke / Sato, Takuma / Miyazawa, Ken / Goto, Shigemi / Togari, Akifumi

International journal of molecular sciences

2022 Volume 23, Issue 16

Abstract: The ganglioside GD1a has been reported to promote the differentiation of mesenchymal stem cells to osteoblasts in cell culture systems. However, the involvement of gangliosides, including GD1a, in bone formation in vivo remains unknown; therefore, we ... ...

Abstract	The ganglioside GD1a has been reported to promote the differentiation of mesenchymal stem cells to osteoblasts in cell culture systems. However, the involvement of gangliosides, including GD1a, in bone formation in vivo remains unknown; therefore, we herein investigated their roles in GM2/GD2 synthase-knockout (GM2/GD2S KO) mice without GD1a. The femoral cancellous bone mass was analyzed using three-dimensional micro-computed tomography. A histomorphometric analysis of bone using hematoxylin and eosin (HE) and tartrate-resistant acid phosphatase was performed to examine bone formation and resorption, respectively. Calcein double labeling was also conducted to evaluate bone formation. Although no significant differences were observed in bone mass or resorption between GM2/GD2S KO mice and wild-type (WT) mice, analyses of the parameters of bone formation using HE staining and calcein double labeling revealed less bone formation in GM2/GD2S KO mice than in WT mice. These results suggest that gangliosides play roles in bone formation.
MeSH term(s)	Animals ; Gangliosides ; Mice ; Mice, Knockout ; N-Acetylgalactosaminyltransferases ; Osteoblasts ; Osteogenesis/genetics ; X-Ray Microtomography
Chemical Substances	Gangliosides ; N-Acetylgalactosaminyltransferases (EC 2.4.1.-) ; (N-acetylneuraminyl)-galactosylglucosylceramide N-acetylgalactosaminyltransferase (EC 2.4.1.92)
Language	English
Publishing date	2022-08-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23169044
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Article ; Online: Store-operated calcium entry induced by activation of Gq-coupled alpha1B adrenergic receptor in human osteoblast.

Kodama, Daisuke / Togari, Akifumi

Biochemical and biophysical research communications

2013 Volume 437, Issue 2, Page(s) 239–244

Abstract: Recent studies have revealed that the sympathetic nervous system is involved in bone metabolism. We previously reported that noradrenaline (NA) suppressed K(+) currents via Gi/o protein-coupled alpha1B-adrenergic receptor (α1B-AR) in human osteoblast SaM- ...

Abstract	Recent studies have revealed that the sympathetic nervous system is involved in bone metabolism. We previously reported that noradrenaline (NA) suppressed K(+) currents via Gi/o protein-coupled alpha1B-adrenergic receptor (α1B-AR) in human osteoblast SaM-1 cells. Additionally, it has been demonstrated that the intracellular Ca(2+) level ([Ca(2+)]i) was increased by NA via α1B-AR. In this study, we investigated the signal pathway of NA-induced [Ca(2+)]i elevation by using Ca(2+) fluorescence imaging in SaM-1 cells. NA-induced [Ca(2+)]i elevation was suppressed by pretreatment with a PLC inhibitor, U73122. This suggested that the [Ca(2+)]i elevation was mediated by Gq protein-coupled α1B-AR. On the other hand, NA-induced [Ca(2+)]i elevation was completely abolished in Ca(2+)-free solution, which suggested that Ca(2+) influx is the predominant pathway of NA-induced [Ca(2+)]i elevation. Although the inhibition of K(+) channel by NA caused membrane depolarization, the [Ca(2+)]i elevation was not affected by voltage-dependent Ca(2+) channel blockers, nifedipine and mibefradil. Meanwhile, NA-induced [Ca(2+)]i elevation was abolished following activation of store-operated Ca(2+) channel by thapsigargin. Additionally, the [Ca(2+)]i elevation was suppressed by store-operated channel inhibitors, 2-APB, flufenamate, GdCl3 and LaCl3. These results suggest that Ca(2+) influx through store-operated Ca(2+) channels plays a critical role in the signal transduction pathway of Gq protein-coupled α1B-AR in human osteoblasts.
MeSH term(s)	Adult ; Calcium/metabolism ; Cells, Cultured ; GTP-Binding Protein alpha Subunits, Gq-G11/metabolism ; Humans ; Male ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Receptors, Adrenergic, alpha-1/metabolism
Chemical Substances	Receptors, Adrenergic, alpha-1 ; GTP-Binding Protein alpha Subunits, Gq-G11 (EC 3.6.5.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2013-07-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2013.06.047
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Article ; Online: Bidirectional communication between sensory neurons and osteoblasts in an in vitro coculture system.

Kodama, Daisuke / Hirai, Takao / Kondo, Hisataka / Hamamura, Kazunori / Togari, Akifumi

FEBS letters

2017 Volume 591, Issue 3, Page(s) 527–539

Abstract: Recent studies have revealed that the sensory nervous system is involved in bone metabolism. However, the mechanism of communication between neurons and osteoblasts is yet to be elucidated. In this study, we investigated the signaling pathways between ... ...

Abstract	Recent studies have revealed that the sensory nervous system is involved in bone metabolism. However, the mechanism of communication between neurons and osteoblasts is yet to be elucidated. In this study, we investigated the signaling pathways between sensory neurons of the dorsal root ganglion (DRG) and the osteoblast-like MC3T3-E1 cells using an in vitro coculture system. Our findings indicate that signal transduction from DRG-derived neurons to MC3T3-E1 cells is suppressed by antagonists of the AMPA receptor and the NK
MeSH term(s)	Adenosine Triphosphate/pharmacology ; Animals ; Bradykinin/pharmacology ; Calcium/metabolism ; Cell Communication/drug effects ; Cell Line ; Coculture Techniques/methods ; Exocytosis/drug effects ; Ganglia, Spinal/cytology ; Glutamic Acid/metabolism ; Humans ; Mice, Inbred BALB C ; Neurotransmitter Agents/metabolism ; Osteoblasts/cytology ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Sensory Receptor Cells/cytology ; Sensory Receptor Cells/drug effects ; Sensory Receptor Cells/metabolism ; Signal Transduction/drug effects ; Substance P/metabolism
Chemical Substances	Neurotransmitter Agents ; Substance P (33507-63-0) ; Glutamic Acid (3KX376GY7L) ; Adenosine Triphosphate (8L70Q75FXE) ; Bradykinin (S8TIM42R2W) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2017-02
Publishing country	England
Document type	Letter
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1002/1873-3468.12561
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Article: Effects of a β2-adrenergic receptor blocker on experimental periodontitis in spontaneously hypertensive rats

Takeguchi, Atsushi / Miyazawa, Ken / Sato, Takuma / Tabuchi, Masako / Muramatsu, Ryujiro / Maeda, Hatsuhiko / Togari, Akifumi / Goto, Shigemi

Life sciences. 2021 July 15, v. 277

2021

Abstract: Recent studies have reported a relationship between periodontal disease and hypertension, and previous evidence suggests that the sympathetic nervous system plays an important role in the control of bone metabolism. This study sought to evaluate the ... ...

Abstract	Recent studies have reported a relationship between periodontal disease and hypertension, and previous evidence suggests that the sympathetic nervous system plays an important role in the control of bone metabolism. This study sought to evaluate the effect of the beta-2 adrenergic receptor (β2-AR) blocker butoxamine on experimental periodontitis in a rat model.Wistar-Kyoto and spontaneously hypertensive rats (n = 6 per group) were orally administered butoxamine 1 mg/kg/day and experimental periodontitis was induced by applying an orthodontic ligature wire. The rats were sacrificed after 4 weeks and the residual alveolar bone was measured using micro-computed tomography (micro-CT) imaging analysis software for histological analysis.Micro-CT imaging analysis showed a higher ratio of residual alveolar bone, BV/TV, and Tb.N in both Wistar-Kyoto and spontaneously hypertensive rats treated with butoxamine compared with the corresponding control rats. In histological analysis, compared with the Wistar-Kyoto and spontaneously hypertensive rat control groups, the corresponding butoxamine-treated groups showed a lower ratio of attachment level, lower values of osteoclast number and surface.β2-AR blockers maintained the alveolar bone mass and attachment level by suppressing osteoclast activity. Thus, β2-AR blockers may be effective in preventing periodontitis.
Keywords	beta-2 adrenergic receptors ; bone density ; bone metabolism ; computer software ; histology ; hypertension ; micro-computed tomography ; osteoclasts ; periodontitis ; rats ; sympathetic nervous system
Language	English
Dates of publication	2021-0715
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.119593
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