Endothelium

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This article is about the lining of blood and lymphatic vessels. For the endothelium of the cornea, see corneal endothelium.
Endothelium
Endotelijalna ćelija.jpg
Diagram showing the location of endothelial cells
Microvessel.jpg
Endothelial cells, which form the tunica intima, or innermost layer of the vessel, encircle an erythrocyte (E).
Code TH H2.00.02.0.02003
Anatomical terminology

The endothelium is the thin layer of cells that lines the interior surface of blood vessels and lymphatic vessels,[1] forming an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. The cells that form the endothelium are 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.

Vascular endothelial cells line the entire circulatory system, from the heart to the smallest capillaries. These cells have unique functions in vascular biology. These functions include fluid filtration, such as in the glomeruli of the kidney, blood vessel tone, hemostasis, neutrophil recruitment, and hormone trafficking. Endothelium of the interior surfaces of the heart chambers is called endocardium.

Structure[edit]

It is mesodermal in 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.[2][3]

Terminology[edit]

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 separate these from epithelial cells.[4] Many considered the endothelium a specialized epithelial tissue.

Function[edit]

Endothelial cells are involved in many aspects of vascular biology, including:

  • Barrier function - the endothelium acts as a semi-selective barrier between the vessel lumen and surrounding tissue, controlling the passage of materials and the transit of white blood cells into and out of the bloodstream. Excessive or prolonged increases in permeability of the endothelial monolayer, as in cases of chronic inflammation, may lead to tissue edema/swelling.
  • Blood clotting (thrombosis & fibrinolysis). The endothelium normally provides a non-thrombogenic surface because it contains, for example, heparan sulfate which acts as a cofactor for activating antithrombin, a protease that inactivates several factors in the coagulation cascade.
  • Inflammation
  • Formation of new blood vessels (angiogenesis)
  • Vasoconstriction and vasodilation, and hence the control of blood pressure
  • Repair of damaged or diseased organs via an injection of blood vessel cells[5]
  • Angiopoietin-2 works with VEGF to facilitate cell proliferation and migration of endothelial cells

Clinical significance[edit]

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. 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.[6] The signalling protein ERK5 is essential for maintaining normal endothelial cell function.[7] 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.

See also[edit]

References[edit]

  1. ^ "Endothelium" at Dorland's Medical Dictionary
  2. ^ Eskin S.G., C.L. Ives, L.V. McIntire, L.T. Navarro. Microvascular Research. Volume 28, Issue 1, July 1984, Pages 87–94Response of cultured endothelial cells to steady flow. http://dx.doi.org/10.1016/0026-2862(84)90031-1
  3. ^ B L Langille and S L Adamson. Relationship between blood flow direction and endothelial cell orientation at arterial branch sites in rabbits and mice. Circulation Research.1981; 48: 481-488.
  4. ^ "FMA". Retrieved 2013-09-28. 
  5. ^ [1]
  6. ^ Deanfield J, Donald A, Ferri C, Giannattasio C, Halcox J, Halligan S, Lerman A, Mancia G, Oliver JJ, Pessina AC, Rizzoni D, Rossi GP, Salvetti A, Schiffrin EL, Taddei S, Webb DJ (January 2005). "Endothelial function and dysfunction. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension". J Hypertens 23 (1): 7–17. doi:10.1097/00004872-200501000-00004. PMID 15643116. 
  7. ^ Roberts OL, Holmes K, Müller J, Cross DA, Cross MJ. (Dec 2009). "ERK5 and the regulation of endothelial cell function". Biochem Soc Trans. 37 (6): 1254–9. doi:10.1042/BST0371254. PMID 19909257. 

External links[edit]