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The glycocalyx (pl.: glycocalyces or glycocalyxes), also known as the pericellular matrix and sometime cell coat, is a glycoprotein and glycolipid covering which surrounds the cell membranes of bacteria, epithelial cells, and other cells. It was described in a review article in 1970. Animal epithelial cells have a fuzz-like coating on the external surface of their plasma membranes. This viscous coating is the glycocalyx that consists of several carbohydrate moieties of membrane glycolipids and glycoproteins, which serve as backbone molecules for support. Generally, the carbohydrate portion of the glycolipids found on the surface of plasma membranes helps these molecules contribute to cell–cell recognition, communication, and intercellular adhesion. The glycocalyx is a type of identifier that the body uses to distinguish between its own healthy cells and transplanted tissues, diseased cells, or invading organisms. Included in the glycocalyx are cell-adhesion molecules that enable cells to adhere to each other and guide the movement of cells during embryonic development. The glycocalyx plays a major role in regulation of endothelial vascular tissue, including the modulation of red blood cell volume in capillaries. The term was initially applied to the polysaccharide matrix coating epithelial cells, but its functions have been discovered to go well beyond that. In vascular endothelial tissue The glycocalyx is located on the apical surface of vascular endothelial cells which line the lumen. When vessels are stained with cationic dyes such as Alcian blue stain, transmission electron microscopy shows a small, irregularly shaped layer extending approximately 50–100 nm into the lumen of a blood vessel. Another study used osmium tetroxide staining during freeze substitution, and showed that the endothelial glycocalyx could be up to 11 μm thick. It is present throughout a diverse range of microvascular beds (capillaries) and macrovessels (arteries and veins). The glycocalyx also consists of a wide range of enzymes and proteins that regulate leukocyte and thrombocyte adherence, since its principal role in the vasculature is to maintain plasma and vessel-wall homeostasis. These enzymes and proteins include: Endothelial nitric oxide synthase (endothelial NOS) Extracellular superoxide dismutase (SOD3) Angiotensin converting enzyme Antithrombin-III Lipoprotein lipase Apolipoproteins Growth factors Chemokines The enzymes and proteins listed above serve to reinforce the glycocalyx barrier against vascular and other diseases. Another main function of the glycocalyx within the vascular endothelium is that it shields the vascular walls from direct exposure to blood flow, while serving as a vascular permeability barrier. Its protective functions are universal throughout the vascular system, but its relative importance varies depending on its exact location in the vasculature. In microvascular tissue, the glycocalyx serves as a vascular permeability barrier by inhibiting coagulation and leukocyte adhesion. Leukocytes must not stick to the vascular wall because they are important components of the immune system that must be able to travel to a specific region of the body when needed. In arterial vascular tissue, the glycocalyx also inhibits coagulation and leukocyte adhesion, but through mediation of shear stress-induced nitric oxide release. Another protective function throughout the cardiovascular system is its ability to affect the filtration of interstitial fluid from capillaries into the interstitial space. The glycocalyx, which is located on the apical surface of endothelial cells, is composed of a negatively charged network of proteoglycans, glycoproteins, and glycolipids. Along the luminal surface of the vascular glycocalyx exists an empty layer that excludes red blood cells. Disruption and disease Because the glycocalyx is so prominent throughout the cardiovascular system, disruption to this structure has detrimental effects that can cause disease. Certain stimuli that cause atheroma may lead to enhanced sensitivity of vasculature. Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized low-density lipoproteins (LDLs), which then causes atherothrombosis. In microvasculature, dysfunction of the glycocalyx leads to internal fluid imbalance, and potentially edema. In arterial vascular tissue, glycocalyx disruption causes inflammation and atherothrombosis. Experiments have been performed to test precisely how the glycocalyx can be altered or damaged. One particular study used an isolated perfused heart model designed to facilitate detection of the state of the vascular barrier portion, and sought to cause insult-induced shedding of the glycocalyx to ascertain the cause-and-effect relationship between glycocalyx shedding and vascular permeability. Hypoxic perfusion of the glycocalyx was thought to be sufficient to initiate a degradation mechanism of the endothelial barrier. The study found that flow of oxygen throughout the blood vessels did not have to be completely absent (ischemic hypoxia), but that minimal levels of oxygen were sufficient to cause the degradation. Shedding of the glycocalyx can be triggered by inflammatory stimuli, such as tumor necrosis factor-alpha. Whatever the stimulus is, however, shedding of the glycocalyx leads to a drastic increase in vascular permeability. Vascular walls being permeable is disadvantageous, since that would enable passage of some macromolecules or other harmful antigens. Other sources of damage to the endothelial glycocalyx have been observed in several pathological conditions such as inflammation, hyperglycemia, ischemia-reperfusion, viral infections and sepsis. Some key components of the glycocalyx such as syndecans, heparan sulphate, chondroitin sulphate and hyaluronan can be shed of the endothelial layer by enzymes. Hyaluronidase, hepararanse/heparinase, matrix and membrane-type matrix metalloproteases, thrombin, plasmin and elastase are some examples of enzymes that can induce shedding of the glycocalyx and these sheddases can therefor contribute to degradation of the glycocalyx layer in several pathological conditions. Research shows that plasma hyaluronidase activity is decreased in experimental as well as in clinical septic shock and is therefore not considered to be a sheddase in sepsis. Concomitant, the endogenous plasma inhibition of hyaluronidase is increased and could serve as a protection against glycocalyx shedding. Fluid shear stress is also a potential problem if the glycocalyx is degraded for any reason. This type of frictional stress is caused by the movement of viscous fluid (i.e. blood) along the lumen boundary. Another similar experiment was carried out to determine what kinds of stimuli cause fluid shear stress. The initial measurement was taken with intravital microscopy, which showed a slow-moving plasma layer, the glycocalyx, of 1 μm thick. Light dye damaged the glyco.... Discover the Max Nieuwdorp popular books. Find the top 100 most popular Max Nieuwdorp books.