The correct physiological functioning of the cardiovascular system depends on complex and exquisite interactions among the cells of the blood vessel wall and between these cells and the cellular and biochemical components of circulating blood. Research in the Department of Vascular Biology and Inflammation (VBI) is aimed at understanding these interactions, how they vary between different vascular beds, and how they are altered in different physiological and pathological situations. At the root of most cardiovascular diseases lies a dysfunction of the endothelium resulting from local injury or an accumulation of deleterious molecules (e.g., oxidized lipoproteins). Damaged vascular cells initiate an inflammatory reaction by releasing vasoactive factors, such as nitric oxide, reactive oxygen species and prostanoids. These factors, together with changes to the expression of cell-surface adhesion molecules, attract circulating leukocytes that bind to and traverse the vessel wall to invade the subendothelial space. The interactions between leukocytes and vascular cells involve cell adhesion, polarization and migration; the release of soluble factors (inflammatory cytokines and chemokines); and extracellular proteolysis. The outcome is a radically altered vascular phenotype characterized by the accumulation of tissue macrophages, tissue remodelling, angiogenesis, and both proliferation and apoptosis of endothelial and smooth muscle cells.

Since its creation, the VBI Department has been closely involved in the general operation of the CNIC, carrying out numerous activities aimed at improving and streamlining research activity. Groups within the department use a range of animal, tissue, cellular and molecular approaches to define normal vascular function and the key steps in vascular alterations that underlie cardiovascular diseases. The department currently has groups working in the following areas:

• Intercellular communication in the inflammatory response: adaptive immune responses and regulatory molecules in chronic vascular inflammation and autoimmune diseases.
• Signalling by adhesion receptors, inflammatory cytokines, chemokines and vasoactive prostaglandins and their receptors.
• Regulation of gene expression in vascular endothelium. Calcium-dependent transcription in brain ischemia.
• Matrix metalloproteinases in angiogenesis and inflammation.
• Endothelial cell junctions and permeability.
• Animal models for the study of basic vascular biology and chronic immune inflammatory diseases (autoimmune myocarditis, atherosclerosis) 

In the coming years, the department intends to recruit new group leaders to lead research groups in the following areas:

• Transduction of mechanical shear stress and vascular distension into intracellular signals, apoptosis in vascular disease, and the role of apoptosis in the formation of atheromatous plaques.
• Animal models for the study of basic vascular disease (arterial hypertension and ventricular hypertrophy).
• Identification of novel therapeutic targets, and the development of new diagnostic and therapeutic tools

In summary, the VBI Department’s main goal is to secure a position as a national and international leader in research in cell biology of the vascular system and in inflammatory physiology and pathology, the root causes of atherothrombotic disease. In the near future, the department will establish an HCS (HTS/HCA) system for massive gene screening and analysis—now that systems biology is becoming attainable. The CNIC is taking the opportunity to become a pioneer in this field.