ACAR
Arterial Calcification & Arterial Regeneration ‘ACAR’
| Coordinatore | WATERFORD INSTITUTE OF TECHNOLOGY
Organization address
address: CORK ROAD contact info |
| Nazionalità Coordinatore | Ireland [IE] |
| Totale costo | 75˙000 € |
| EC contributo | 75˙000 € |
| Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | FP7-PEOPLE-2011-CIG |
| Funding Scheme | MC-CIG |
| Anno di inizio | 2011 |
| Periodo (anno-mese-giorno) | 2011-12-01 - 2014-11-30 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
WATERFORD INSTITUTE OF TECHNOLOGY
Organization address
address: CORK ROAD contact info |
IE (WATERFORD) | coordinator | 75˙000.00 |
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Obiettivo del progetto (Objective)
'Arterial calcification is a morbid complication of inflammatory disease causing calcium deposition along arterial walls. Sheer stresses on cellular components affect regenerative capabilities of specific cells, culminating in vessel constriction, compromised wall elasticity and reduced blood flow. The net effect of restricted blood flow is debilitating and can cause cardiovascular disease, end stage renal disease or peripheral arterial disease. Animal models have uncovered biomarkers involved in calcification however little is known in humans. Therefore we will investigate two calcification mechanisms believed to play a role; warfarin, an anticoagulant and inducer of calcification in certain cells and oxidative stress which impacts on cellular mechanisms increasing calcification status. Firstly, we will demonstrate that stress induced calcification biomarkers are deregulated in vascular smooth muscle cells. We will identify novel biomarkers involved in this process. We will also investigate calcification reversal using vitamin K and selenium supplementation in these cells by monitoring calcification biomarker expression. Secondly, we will investigate the regenerative capabilities of endothelial progenitor cells in peripheral arterial disease, a serious inflammatory disease. From patients and controls, we will isolate endothelial progenitor cells and compare biomarker expression using cell culture assays which will be developed in the laboratory. This research project fulfils several objectives. Firstly, it facilitates reintegration of the researcher allowing him to establish cell culturing facilities in the host laboratory. Secondly, it allows for the investigation and identification of calcification biomarkers in human cells and cellular mechanisms to combat this and finally to investigate the regenerative capabilities of endothelial progenitor cells in subjects. This research could establish mechanistic paradigms implicated in other inflammatory diseases.'