eCM (Eur Cell Mater / e Cells & Materials) Not-for-profit Open Access
Created by Scientists, for Scientists
 ISSN:1473-2262         NLM:100973416 (link)         DOI:10.22203/eCM

2004   Volume No 7- pages 12-26

Title: Glutamate signalling and its potential application to tissue engineering of bone

Author: Deborah J. Mason

Address: School of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3US, U.K

E-mail: masondj at

Key Words: Glutamate, bone tissue engineering, glutamate transporters, glutamate receptors, osteocytes, osteoblasts, osteoclasts, ion channels, mechanical load.

Publication date: April 7th 2004

Abstract: Mechanical loading of the skeleton is important for maintenance of adequate bone mass and defined mechanical stimuli are highly osteogenic. The identification of mechanoresponsive signalling molecules in bone may allow osteogenic signals to be mimicked. This approach would be useful in the treatment of bone pathologies where the skeleton is too weak to withstand osteogenic forces and to tissue engineering of bone where the mechanical environment of bone cells is disrupted. Glutamate has been implicated as a mediator of mechanical signalling in bone. Evidence for glutamate signalling in bone, its role in mechanotransduction and potential applications of this pathway to tissue engineering of bone is considered in this review. Glutamate receptors, transporters and proteins that regulate glutamate release, are all expressed in bone cells. Glutamate receptor activation affects both osteoblast and osteoclast phenotypes revealing a potential for therapeutic manipulation of glutamate signalling to enhance bone formation. Glutamate transporters contribute to this system by regulating extracellular glutamate concentrations and acting as glutamate-gated ion channels. Artificial regulation of glutamate receptors or transporters may be used to increase the bone forming capacity of osteoblasts. This novel approach may potentially enhance bone tissue engineering strategies.

Article download: Pages 12-26. (PDF file)
DOI: 10.22203/eCM.v007a02