Abstract
Cardiovascular diseases are a group of disorders caused by the presence of a combination of risk factors, such as tobacco use, unhealthy diet and obesity, physical inactivity, etc., which cause the modification of the composition of the vessel’s matrix and lead to the alteration of blood flow, matched with an inflammation condition. Nevertheless, it is not clear if the inflammation is a permissive condition or a consequent one. In order to investigate the effect of inflammation on the onset of vascular disease, we treated endothelial cells with the cytokine TNF-α that is increased in obese patients and is reported to induce cardiometabolic diseases. The inflammation induced a large change in the extracellular matrix, increasing the pericellular hyaluronan and altering the heparan sulfate Syndecans sets, which seems to be related to layer permeability but does not influence cell proliferation or migration nor induce blood cell recruitment or activation.
Highlights
Cardiovascular diseases (CVD) are a group of pathologies of the vascular system that are growing in number and that usually present a build-up of fatty deposits inside the arteries and an increased risk of blood clots and can be associated with damage to arteries in organs such as the brain, heart, kidneys, and eyes
In order to confirm the inflammatory condition of Human umbilical vein endothelial cells (HUVEC) cells, we analyzed nitric oxide synthases (NOSs) expression
The endothelial isoform NOS3 was the most expressed form in HUVEC (Figure 1A), and the expression levels of NOS3 and NOS1 were significantly decreased after TNF-α stimulation, while NOS2 showed a non-significant tendency to decrease (Figure 1B)
Summary
Cardiovascular diseases (CVD) are a group of pathologies of the vascular system that are growing in number and that usually present a build-up of fatty deposits inside the arteries (atherosclerosis) and an increased risk of blood clots and can be associated with damage to arteries in organs such as the brain, heart, kidneys, and eyes. Some authors proposed that some of the risk factors lead to qualitative changes in the endothelium such as changes in permeability and increase in adhesion molecules expression that attract leucocytes (“response of injury” hypothesis) [5,6], which, in turn, cause the inflammatory condition. The localized inflammation causes the thickening of the arterial wall due to the increased deposition of extracellular matrix (ECM) and the newly formed ECM traps lipoprotein and inflammatory/growth factors from the circulation within the vessel wall [3]
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