Vulnerable Atherosclerotic Plaques, Foam Cell Phenotypes & Extracellular Proteinases

  • Tsaousi, Aikaterini (Co-Investigator)
  • Hayes, Elaine M (Co-Investigator)
  • Bevan, Laura A (Technician)
  • Thomas, Anita C (Co-Investigator)
  • Newby, Andrew C (Principal Investigator)

Project Details

Description

Coronary heart disease is caused by obstruction of the arteries feeding the heart thanks to a build up of fatty deposits known as atherosclerotic plaques. Heart attacks are often caused by blood clots forming at the point where plaques rupture because they have become weakened by digestive enzymes called proteases. White blood cells enter plaques initially to get rid of the fatty deposits but can become trapped. Our recent work shows that white blood cells often over-produce proteases in this situation and therefore change from beneficial to harmful. This programme seeks to find ways of reversing this process and thereby prevent heart attacks.

Key findings

Rag KO does not influence macrophage polarization or MMP expression during atherosclerosis. Tbet KO reduces atherosclerotic plaque size but not plaque vulnerability to rupture, as M1 polarization and related MMP expression is maintained.
AcronymBHF Programme Grant RG/04/009 (co-investigator)
StatusFinished
Effective start/end date1/04/1230/09/14

Research Output

  • 1 Article (Academic Journal)

Classical and Alternative Activation and Metalloproteinase Expression Occurs in Foam Cell Macrophages in Male and Female ApoE Null Mice in the Absence of T and B Lymphocytes

Hayes, E. M., Tsaousi, A., Di Gregoli, K., Jenkinson, S. R., Bond, A. R., Johnson, J. L., Bevan, L. A., Thomas, A. C. & Newby, A. C., 28 Oct 2014, In : Frontiers in Immunology. 5, 16 p., 537.

Research output: Contribution to journalArticle (Academic Journal)

  • 22 Citations (Scopus)
    7 Downloads (Pure)