4.6 Article

Plasma haemoxygenase-1 in coronary artery disease A comparison with angiogenin, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1 and vascular endothelial growth factor

Journal

THROMBOSIS AND HAEMOSTASIS
Volume 104, Issue 5, Pages 1029-1037

Publisher

GEORG THIEME VERLAG KG
DOI: 10.1160/TH09-11-0802

Keywords

Haemoxygenase 1 angiogenin matrix metalloproteinase 9; tissue inhibitor of metalloproteinase; vascular endothelial growth factor; coronary artery disease

Funding

  1. Sandwell and West Birmingham Hospitals
  2. NHS Trust Research and Development Unit
  3. Egyptian Government

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It was the aim of this study to determine plasma haemoxygenase 1 (HO 1) across the spectrum of health, angina but normal coronary arteries (NCA) stable coronary artery disease (CAD) and acute coronary syndromes (ACS) and relationships with angiogenin matrix metallo proteinase 9 (MMP 9), tissue inhibitor of metalloproteinase 1, and vascular endothelial growth factor Plasma markers were measured (ELISA) in peripheral venous citrated plasma from 50 healthy subjects 30 with NCA, 70 with stable CAD and 24 with an ACS and from patient s aortic root coronary ostium coronary sinus and femoral artery Human umbilical vein endothelial cells (HUVECs) were cultured with or without tumour necrosis factor (TNF) and platelets were probed HO 1 was raised in stable CAD (p<0 05) and increased further in ACS (p<0 01) compared to healthy controls and NCA HO 1 correlated only with, MMP 9, and then only in the healthy controls There were no major differences from cardiac or peripheral sites HO 1 was present in HUVECs and 24 hour HUVEC supernatants but release was abolished by TNF Platelets had no HO 1 In conclusion, HO 1 is raised in stable CAD and ACS and may arise from the endothelium but not the platelet This may have implications for our understanding of the pathophysiology of CAD and its acute presentation as ACS

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