Endothelium

Endothelium refers to cells that line the interior surface of blood vessels and lymphatic vessels, forming an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. It is a thin layer of simple, or single-layered, squamous cells called endothelial cells. Endothelial cells in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells.

Endothelium is of mesodermal origin. Both blood and lymphatic capillaries are composed of a single layer of endothelial cells called a monolayer. In straight sections of a blood vessel, vascular endothelial cells typically align and elongate in the direction of fluid flow.

The foundational model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence of vimentin rather than keratin filaments separates these from epithelial cells. Many considered the endothelium a specialized epithelial tissue.

Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and is often regarded as a key early event in the development of atherosclerosis. Impaired endothelial function, causing hypertension and thrombosis, is often seen in patients with coronary artery disease, diabetes mellitus, hypertension, hypercholesterolemia, as well as in smokers. Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events, and is also present in inflammatory disease such as rheumatoid arthritis and systemic lupus erythematosus.

Endothelial dysfunction is a result of changes in endothelial physiology. In response to lipid accumulation and proinflammatory stimuli, endothelial cells become activated, which is characterized by the expression of adhesion molecules such as E-selectin, VCAM-1 and ICAM-1. Additionally, transcription factors including AP-1 and NF-kB become activated, leading to up-regulated expression of proinflammatory cytokines, such as IL-1, TNFa and IFNy. The proatherogenic profile expressed by the endothelial cells promotes accumulation of lipids and lipoproteins in the intima, and subsequent recruitment of leukocytes and platelets, as well as proliferation of smooth muscle cells, leading to fatty streak formation. The lesions formed in the intima, and persistent inflammation lead to desquamation of endothelium, which disrupts the endothelial barrier, leading to injury and consequent dysfunction. In contrast, inflammatory stimuli also activate NF-kB induced expression of the deubiquitinase A20 (TNFAIP3), which has been shown to intrinsically repair the endothelial barrier.

One of the main mechanisms of endothelial dysfunction is the diminishing of nitric oxide, often due to high levels of asymmetric dimethylarginine, which interfere with the normal L-arginine-stimulated nitric oxide synthesis and so leads to hypertension. The most prevailing mechanism of endothelial dysfunction is an increase in reactive oxygen species, which can impair nitric oxide production and activity via several mechanisms. The signalling protein ERK5 is essential for maintaining normal endothelial cell function. A further consequence of damage to the endothelium is the release of pathological quantities of von Willebrand factor, which promote platelet aggregation and adhesion to the subendothelium, and thus the formation of potentially fatal thrombi.

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EPIGENETICS IN BACTERIA

MEDICINE AND EPIGENETICS

PSYHOLOGY AND PSYCHIATRY OF EPIGENETICS

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