PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10459768

Pertussis toxin-sensitive G proteins as mediators of stretch-induced decrease in nitric-oxide release of osteoblast-like cells.

F Hara·K Fukuda·M Ueno·C Hamanishi·S Tanaka
View original source ↗Export metadata ↓

Abstract

Mechanical loading plays an important role in regulating bone remodeling, and nitric oxide may be one regulator of this process. To determine how mechanical stress modulates osteoblast function, we loaded cyclic tensile stretch on osteoblast-like cells and measured levels of nitric oxide in the medium. High frequency of stretch at any magnitude inhibited release of nitric oxide; however, low frequency of stretch enhanced its release from the static control. To examine the involvement of G protein (guanine nucleotide-binding regulatory protein) in stress-inhibited release of nitric oxide, we added pertussis toxin, a specific inhibitor of the Gi class, and found that it completely reversed the stress-inhibited release. These data support the idea that pertussis toxin-sensitive G protein is activated in the presence of cyclic tensile stretch.

Explore related subjects

Bone RemodelingGTP-Binding ProteinsNitric OxideOsteoblastsPertussis ToxinStress, MechanicalTumor Cells, CulturedVirulence Factors, BordetellaJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

F Hara, K Fukuda, M Ueno, C Hamanishi, S Tanaka. 1999. Pertussis toxin-sensitive G proteins as mediators of stretch-induced decrease in nitric-oxide release of osteoblast-like cells.. https://doi.org/10.1002/jor.1100170420

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Long-term potentiation in bone--a role for glutamate in strain-induced cellular memory?

BACKGROUND: The adaptive response of bone cells to mechanical strain is a primary determinant of skeletal architecture and bone mass. In vivo mechanical loading induces new bone formation and increases bone mineral density whereas disuse, immobilisation and weightlessness induce bone loss. The potency of mechanical strain is such that a single brief period of loading at physiological strain magnitude is able to induce a long-lasting osteogenic response that lasts for days. Although the process of mechanotransduction in bone is incompletely understood, observations that responses to mechanical strain outlast the duration of stimulation necessitate the existence of a form of cellular memory through which transient strain episodes are recorded, interpreted and remembered by bone cells. Recent evidence supports the existence of a complex multicellular glutamate-signalling network in bone that shares functional similarities to glutamatergic neurotransmission in the central nervous system. In neurones, these signalling molecules coordinate synaptic communication required to support learning and memory formation, through a complex process of long-term potentiation. PRESENTATION OF THE HYPOTHESIS: We hypothesise that osteoblasts use a cellular mechanism similar or identical to neuronal long-term potentiation in the central nervous system to mediate long-lasting changes in osteogenesis following brief periods of mechanical strain. TESTING THE HYPOTHESIS: N-methyl-D-aspartate (NMDA) receptor antagonism should inhibit the saturating response of mechanical strain and reduce the enhanced osteogenicity of segregated loading to that of an equivalent period of uninterrupted loading. Changes in alpha-amino-3-hydroxy-5-methyl-isoxazole propionate (AMPA) receptor expression, localisation and electrophysiological responses should be induced by mechanical strain and inhibited by modulators of neuronal long-term potentiation. IMPLICATIONS OF THE HYPOTHESIS: If true, this hypothesis would provide a mechanism through which the skeleton could be pharmacologically primed to enhance or retrieve the normal osteogenic response to exercise. This would form a basis through which novel therapies could be developed to target osteoporosis and other prevalent bone disorders associated with low bone mass.

Bone Remodeling↗
PubMed2003

Fronto-orbital remodeling without orbito-naso-frontal bandeau.

INTRODUCTION: Fronto-orbital bilateral advance is the procedure of choice for the treatment of craniosynostosis affecting most of the anterior area of the skull and orbitomalar regions. The aim of the technique is to achieve a supra-orbital bilateral bar and a frontal bone. We have introduced a modification in order to simplify the technique. PATIENTS AND METHODS: From November 1998 to January 2002, 18 patients with craniosynostosis have been surgically treated using our technique. The mean age when the treatment was performed was 6.93 months (range 3 to 22 months). Brain computed tomography (CT) scans and three-dimensional (3-D) reconstruction of CT scans were performed before and after treatment. SURGICAL TECHNIQUE: A bifrontal craniotomy was performed taking the osteotomy up to the supraorbital rim. A new frontal bone was obtained from another region of the cranium creating new orbital edges. The osteosynthesis was conducted using absorbable materials. RESULTS: The follow-up of the patients ranged from 3 months to 3 years. All patients were studied using CT scans and 3-D reconstruction of CT after treatment, which demonstrated the persistence of the fronto-orbital advance. No secondary complications related to the new technique were found in any of the patients. CONCLUSIONS: The frontal-orbital advance obtained was stable. The technique was simplified by not creating a supraorbital bar and by reducing the bone fixation points. The manipulation of both frontal lobes and orbital globes was negligible. The aesthetic results were excellent.

Bone Remodeling↗