Endothelium

This article is about the lining of blood and lymphatic vessels. For the endothelium of the cornea, see corneal endothelium.
Endothelium

Diagram showing the location of endothelial cells

Endothelial cells, which form the tunica intima, or innermost layer of the vessel, encircle an erythrocyte (E).
Identifiers
Code TH H2.00.02.0.02003

Anatomical terminology

Endothelium is a type of epithelium 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. It is a thin layer of simple 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.

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

Endothelium 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

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.[5]

Function

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

Clinical significance

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.[8] The signalling protein ERK5 is essential for maintaining normal endothelial cell function.[9] 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.

Additional images

Endothelium lines the inner wall of vessels, shown here.

See also

References

  1. ↑ "Endothelium" at Dorland's Medical Dictionary
  2. ↑ Eskin, S.G.; Ives, C.L.; McIntire, L.V.; Navarro, L.T. "Response of cultured endothelial cells to steady flow". Microvascular Research 28 (1): 87–94. doi:10.1016/0026-2862(84)90031-1.
  3. ↑ Langille, B L; Adamson, S L (1981). "Relationship between blood flow direction and endothelial cell orientation at arterial branch sites in rabbits and mice". Circulation Research 48: 481–488. doi:10.1161/01.res.481.
  4. ↑ "FMA". Retrieved 2013-09-28.
  5. ↑ Kovacic, Jason; Mercader, Nadia; Torres, Miguel; Boehm, Manfred; Fuster, Valentin (2012). "Cardiovascular Development to Disease Epithelial-to-Mesenchymal and Endothelial-to-Mesenchymal Transition: From Cardiovascular Development to Disease". Circulation 125: 1795–1808. doi:10.1161/circulationaha.111.040352. Retrieved 8 November 2014.
  6. ↑ Li X, Fang P, et al. (April 2016). "Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-Induced Endothelial Cell Activation". Arteriosclerosis, Thrombosis, and Vascular Biology. doi:10.1161/ATVBAHA.115.306964. PMID 27127201.
  7. ↑
  8. ↑ 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.
  9. ↑ 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

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