Award details

MRC DTA Studentship: Physiological and pathological roles of InsP3 in cardiac myocytes

Reference	BBS/E/B/0000M975
Principal Investigator / Supervisor	Dr Martin Bootman
Co-Investigators / Co-Supervisors
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	44,103
Status	Completed
Type	Institute Project
Start date	01/10/2004
End date	30/09/2007
Duration	36 months

Abstract

The cyclical contraction of the heart pumps blood around the lungs and the body. There is a precise order of electrical events that spread from a pacemaking centre (the sinoatrial node) through the atria to ventricles. Disturbances in the spread of the electrical signal, or occurrence of a spontaneous electrical signal, can lead to fatal corruption of the heart¿s function. Calcium underlies the contraction of cardiac cells. As the electrical signal sweeps through the heart, calcium channels open in its wake. The increase in calcium within cardiac myocytes causes them to contract. The simultaneous recruitment of many cells generates the force required to pump blood. Increases of calcium within cardiac cells occur following opening channels located on the outer membrane of the cells and also on internal stores. Many of the proteins involved in generating and regulating calcium signals have been identified and at least partially characterised. The heart is a complex organ and it has the capacity to remodel during periods of intense activity or hormonal stimulation. In some situations, the adaptation of the heart is beneficial and reversible, such as during aerobic training. However, some remodelling is not helpful and can lead to irreversible changes in the ability of the heart to pump blood. This project seeks to characterise the role of inositol 1,4,5-trisphosphate receptors (InsP3Rs) in heart function. InsP3Rs are calcium channels that exist in a number of cell types throughout the body, and play a critical role in generating signals underlying memory, gene transcript and regulating metabolism. Although InsP3Rs are known to be expressed in the heart, their role is not well understood. Our previous work has shown the adult atrial myocytes abundantly express InsP3Rs, and that these channels have the capacity to increase the contractile force of the cells, but also to cause spontaneous calcium signals that may lead to arrhythmic heart beats.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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