Overexpression of hypoxia/inflammatory markers in atherosclerotic carotid plaques.

2008, Front Biosci. 2008 May 1;13:6483-90.
Luque A, Turu M, Juan-Babot O, Cardona P, Font A, Carvajal A, Slevin M, Iborra E, Rubio F, Badimon L, Krupinski J.
Autors del centre relacionats: Badimon Lina, Juan Oriol, Slevin Mark.

Hypoxia, angiogenesis and inflammation leads to plaque progression and remodelling and may significantly contribute towards plaque rupture and subsequent cerebrovascular events. Our aim was to study, markers of hypoxia and inflammation previously identified by microarray analysis, in atherosclerotic carotid arteries with low to moderate stenosis. We hoped to describe different cellular populations expressing the studied markers. The location of selected inflammatory molecules obtained as vascular transplants from organ donors were analysed by immunohistochemistry with monoclonal and polyclonal antibodies. Paraffin-embedded sections were cut and probed with antibodies recognizing active B and T-lymphocytes (CD30), hypoxia-inducible factor-1alpha, endoglin (CD105), Interleukin-6 and C-reactive protein. We observed a notable overexpression of HIF-1alpha in inflammatory and hypoxic areas of carotid arteries in all types of lesions from type II-V taken from the patients with carotid stenosis less than 50%. This suggests that HIF-1alpha may have a putative role in atherosclerosis progression and angiogenesis. Dynamic changes in the non-occluding plaques may explain some of the clinical events in patients with low to moderate carotid stenosis.

We would like to adnowledge the support of the Fundacion BBVA.

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