Glutamate regulation for bone repair

Brakspear, Karen Sarah 2010. Glutamate regulation for bone repair. PhD Thesis, Cardiff University.

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Abstract

Mechanical loading plays a key role in the physiology of bone, allowing bone to functionally adapt to its environment. A screen for genes associated with mechanical load-induced bone formation identified the glutamate transporter GLAST, implicating the excitatory amino acid glutamate in the mechanoresponse. Bone cells express functional components from each stage of the glutamate signalling pathway. Five high affinity Na+-dependent excitatory amino acid transporters (EAATs) terminate glutamatergic signalling. EAAT1 (GLAST) is expressed by osteocytes and bone-forming osteoblasts in vivo, and may influence osteogenesis by regulating glutamate uptake, glutamate release, glutamate-gated ion channel activity or through activation of intracellular signalling pathways. The aim was to assess EAAT expression and function in osteoblasts and determine whether modulation of EAAT activities in osteoblasts influences differentiation and bone forming activity through measurement of cell number, gene expression, alkaline phosphatase (ALP) activity and mineralisation.

Item Type:	Thesis (PhD)
Status:	Unpublished
Schools:	Biosciences
Subjects:	Q Science > Q Science (General)
Funders:	BBSRC, Smith & Nephew
Date of First Compliant Deposit:	30 March 2016
Last Modified:	14 Oct 2019 13:42
URI:	https://orca.cardiff.ac.uk/id/eprint/54184

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