Glycocalyx

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Glycocalyx
Bacillus subtilis.jpg
TEM micrograph of a B. subtilis bacterium, with the hair-like glycocalyx visible surrounding the cell membrane (scale bar = 200 nm)
Identifiers
MeSH D019276
TH H1.00.01.1.00002
FMA 66838
Anatomical terms of microanatomy

The glycocalyx (pl.: glycocalyces or glycocalyxes), also known as the pericellular matrix and sometime cell coat, is a glycoprotein and glycolipid covering that surrounds the cell membranes of bacteria, epithelial cells, and other cells. It was described in a review article in 1970. [1]

Contents

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. [2]

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. [3] The glycocalyx plays a major role in regulation of endothelial vascular tissue, including the modulation of red blood cell volume in capillaries. [4]

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. [5] 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:

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. [6] 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. [7]

The glycocalyx, which is located on the apical surface of endothelial cells, is composed of a negatively charged network of proteoglycans, glycoproteins, and glycolipids. [8] Along the luminal surface of the vascular glycocalyx exists an empty layer that excludes red blood cells. [9]

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. [10]

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[ clarification needed ] 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[ clarification needed ] increase in vascular permeability. Vascular walls being permeable is disadvantageous, since that would enable passage of some macromolecules or other harmful antigens. [11]

Other sources of damage to the endothelial glycocalyx have been observed in several pathological conditions such as inflammation, [12] hyperglycemia, [13] ischemia-reperfusion, [14] viral infections [15] and sepsis. [16]

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. [17] 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. [18] 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 glycocalyx minimally, but that small change increased capillary hematocrit. Thus, fluorescence light microscopy should not be used to study the glycocalyx because that particular method uses a dye. The glycocalyx can also be reduced in thickness when treated with oxidized LDL. [19] These stimuli, along with many other factors, can cause damage to the delicate glycocalyx. These studies are evidence that the glycocalyx plays a crucial role in cardiovascular system health.

In bacteria and nature

The glycocalyx exists in bacteria as either a capsule or a slime layer. Item 6 points at the glycocalyx. The difference between a capsule and a slime layer is that in a capsule polysaccharides are firmly attached to the cell wall, while in a slime layer, the glycoproteins are loosely attached to the cell wall. Glycocalyx in bacteria.svg
The glycocalyx exists in bacteria as either a capsule or a slime layer. Item 6 points at the glycocalyx. The difference between a capsule and a slime layer is that in a capsule polysaccharides are firmly attached to the cell wall, while in a slime layer, the glycoproteins are loosely attached to the cell wall.

A glycocalyx, literally meaning "sugar coat" (glykys = sweet, kalyx = husk), is a network of polysaccharides that project from cellular surfaces of bacteria, which classifies it as a universal surface component of a bacterial cell, found just outside the bacterial cell wall. A distinct, gelatinous glycocalyx is called a capsule, whereas an irregular, diffuse layer is called a slime layer. This coat is extremely hydrated and stains with ruthenium red.

Bacteria growing in natural ecosystems, such as in soil, bovine intestines, or the human urinary tract, are surrounded by some sort of glycocalyx-enclosed microcolony. [20] It serves to protect the bacterium from harmful phagocytes by creating capsules or allowing the bacterium to attach itself to inert surfaces, such as teeth or rocks, via biofilms (e.g. Streptococcus pneumoniae attaches itself to either lung cells, prokaryotes, or other bacteria which can fuse their glycocalices to envelop the colony).

In the digestive tract

A glycocalyx can also be found on the apical portion of microvilli within the digestive tract, especially within the small intestine. It creates a meshwork 0.3 μm thick and consists of acidic mucopolysaccharides and glycoproteins that project from the apical plasma membrane of epithelial absorptive cells. It provides additional surface for adsorption and includes enzymes secreted by the absorptive cells that are essential for the final steps of digestion of proteins and sugars.

Other generalized functions

Related Research Articles

<span class="mw-page-title-main">Biological membrane</span> Enclosing or separating membrane in organisms acting as selective semi-permeable barrier

A biological membrane, biomembrane or cell membrane is a selectively permeable membrane that separates the interior of a cell from the external environment or creates intracellular compartments by serving as a boundary between one part of the cell and another. Biological membranes, in the form of eukaryotic cell membranes, consist of a phospholipid bilayer with embedded, integral and peripheral proteins used in communication and transportation of chemicals and ions. The bulk of lipids in a cell membrane provides a fluid matrix for proteins to rotate and laterally diffuse for physiological functioning. Proteins are adapted to high membrane fluidity environment of the lipid bilayer with the presence of an annular lipid shell, consisting of lipid molecules bound tightly to the surface of integral membrane proteins. The cell membranes are different from the isolating tissues formed by layers of cells, such as mucous membranes, basement membranes, and serous membranes.

<span class="mw-page-title-main">Capillary</span> Smallest type of blood vessel

A capillary is a small blood vessel, from 5 to 10 micrometres in diameter, and is part of the microcirculation system. Capillaries are microvessels and the smallest blood vessels in the body. They are composed of only the tunica intima, consisting of a thin wall of simple squamous endothelial cells. They are the site of the exchange of many substances from the surrounding interstitial fluid, and they convey blood from the smallest branches of the arteries (arterioles) to those of the veins (venules). Other substances which cross capillaries include water, oxygen, carbon dioxide, urea, glucose, uric acid, lactic acid and creatinine. Lymph capillaries connect with larger lymph vessels to drain lymphatic fluid collected in microcirculation.

<span class="mw-page-title-main">Angiogenesis</span> Blood vessel formation, when new vessels emerge from existing vessels

Angiogenesis is the physiological process through which new blood vessels form from pre-existing vessels, formed in the earlier stage of vasculogenesis. Angiogenesis continues the growth of the vasculature mainly by processes of sprouting and splitting, but processes such as coalescent angiogenesis, vessel elongation and vessel cooption also play a role. Vasculogenesis is the embryonic formation of endothelial cells from mesoderm cell precursors, and from neovascularization, although discussions are not always precise. The first vessels in the developing embryo form through vasculogenesis, after which angiogenesis is responsible for most, if not all, blood vessel growth during development and in disease.

<span class="mw-page-title-main">Inflammation</span> Physical effects resulting from activation of the immune system

Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair.

<span class="mw-page-title-main">Microcirculation</span> Circulation of the blood in the smallest blood vessels

The microcirculation is the circulation of the blood in the smallest blood vessels, the microvessels of the microvasculature present within organ tissues. The microvessels include terminal arterioles, metarterioles, capillaries, and venules. Arterioles carry oxygenated blood to the capillaries, and blood flows out of the capillaries through venules into veins.

<span class="mw-page-title-main">Endothelium</span> Layer of cells that lining inner surface of blood vessels

The endothelium is a single layer of squamous endothelial cells that line the interior surface of blood vessels and lymphatic vessels. The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. Endothelial cells form the barrier between vessels and tissue and control the flow of substances and fluid into and out of a tissue.

<span class="mw-page-title-main">Lymphatic vessel</span> Tubular vessels that are involved in the transport of lymph and lymphocytes

The lymphatic vessels are thin-walled vessels (tubes), structured like blood vessels, that carry lymph. As part of the lymphatic system, lymph vessels are complementary to the cardiovascular system. Lymph vessels are lined by endothelial cells, and have a thin layer of smooth muscle, and adventitia that binds the lymph vessels to the surrounding tissue. Lymph vessels are devoted to the propulsion of the lymph from the lymph capillaries, which are mainly concerned with the absorption of interstitial fluid from the tissues. Lymph capillaries are slightly bigger than their counterpart capillaries of the vascular system. Lymph vessels that carry lymph to a lymph node are called afferent lymph vessels, and those that carry it from a lymph node are called efferent lymph vessels, from where the lymph may travel to another lymph node, may be returned to a vein, or may travel to a larger lymph duct. Lymph ducts drain the lymph into one of the subclavian veins and thus return it to general circulation.

<span class="mw-page-title-main">Glomerulus (kidney)</span> Functional unit of nephron

The glomerulus is a network of small blood vessels (capillaries) known as a tuft, located at the beginning of a nephron in the kidney. Each of the two kidneys contains about one million nephrons. The tuft is structurally supported by the mesangium, composed of intraglomerular mesangial cells. The blood is filtered across the capillary walls of this tuft through the glomerular filtration barrier, which yields its filtrate of water and soluble substances to a cup-like sac known as Bowman's capsule. The filtrate then enters the renal tubule of the nephron.

<span class="mw-page-title-main">Leukotriene</span> Class of inflammation mediator molecules

Leukotrienes are a family of eicosanoid inflammatory mediators produced in leukocytes by the oxidation of arachidonic acid (AA) and the essential fatty acid eicosapentaenoic acid (EPA) by the enzyme arachidonate 5-lipoxygenase.

The Starling principle holds that extracellular fluid movements between blood and tissues are determined by differences in hydrostatic pressure and colloid osmotic (oncotic) pressure between plasma inside microvessels and interstitial fluid outside them. The Starling Equation, proposed many years after the death of Starling, describes that relationship in mathematical form and can be applied to many biological and non-biological semipermeable membranes. The classic Starling principle and the equation that describes it have in recent years been revised and extended.

<span class="mw-page-title-main">Glycolipid</span> Class of chemical compounds

Glycolipids are lipids with a carbohydrate attached by a glycosidic (covalent) bond. Their role is to maintain the stability of the cell membrane and to facilitate cellular recognition, which is crucial to the immune response and in the connections that allow cells to connect to one another to form tissues. Glycolipids are found on the surface of all eukaryotic cell membranes, where they extend from the phospholipid bilayer into the extracellular environment.

<span class="mw-page-title-main">Hyaluronidase</span> Class of enzymes

Hyaluronidases are a family of enzymes that catalyse the degradation of hyaluronic acid. Karl Meyer classified these enzymes in 1971, into three distinct groups, a scheme based on the enzyme reaction products. The three main types of hyaluronidases are two classes of eukaryotic endoglycosidase hydrolases and a prokaryotic lyase-type of glycosidase.

<span class="mw-page-title-main">Pericyte</span> Cells associated with capillary linings

Pericytes are multi-functional mural cells of the microcirculation that wrap around the endothelial cells that line the capillaries throughout the body. Pericytes are embedded in the basement membrane of blood capillaries, where they communicate with endothelial cells by means of both direct physical contact and paracrine signaling. The morphology, distribution, density and molecular fingerprints of pericytes vary between organs and vascular beds. Pericytes help to maintain homeostatic and hemostatic functions in the brain, one of the organs with higher pericyte coverage, and also sustain the blood–brain barrier. These cells are also a key component of the neurovascular unit, which includes endothelial cells, astrocytes, and neurons. Pericytes have been postulated to regulate capillary blood flow and the clearance and phagocytosis of cellular debris in vitro. Pericytes stabilize and monitor the maturation of endothelial cells by means of direct communication between the cell membrane as well as through paracrine signaling. A deficiency of pericytes in the central nervous system can cause increased permeability of the blood–brain barrier.

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<span class="mw-page-title-main">Vascular permeability</span>

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<span class="mw-page-title-main">Leukocyte extravasation</span>

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<span class="mw-page-title-main">AOC3</span> Enzyme

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References

  1. ↑ Martínez-Palomo, A. (1970). "The Surface Coats of Animal Cells". International Review of Cytology. 29: 29–75. doi:10.1016/S0074-7696(08)60032-7. ISBN   9780123643292.
  2. ↑ McKinley, M. & V.D. O’Loughlin. Human Anatomy. McGraw-Hill, 2012. 3rd ed. p. 30-31.
  3. ↑ Saladin, Kenneth. "Anatomy & Physiology: The unity of form and function." McGraw Hill. 5th Edition. 2010. p. 94-95
  4. ↑ Reitsma, Sietze. "The endothelial glycocalyx: composition, functions, and visualization." European Journal of Physiology. 2007. Vol. 454. Num. 3. p. 345-359
  5. ↑ Ebong, Eno; Macaluso FP; Spray DC; Tarbell JM (August 2011). "Imaging the Endothelial Glycocalyx In Vitro By Rapid Freezing/Freeze Substitution Transmission Electron Microscopy". Arteriosclerosis, Thrombosis, and Vascular Biology. 31 (8): 1908–1915. doi:10.1161/ATVBAHA.111.225268. PMC   3141106 . PMID   21474821.
  6. ↑ Van de Berg, Bernard M., Max Nieuwdorp, Erik S.G. Stroes, Hans Vink. "Glycocalyx and endothelial (dys) function: from mice to men." Pharmacological Reports, 2006, 57: 75-80.
  7. ↑ Drake-Holland, Angela & Mark Noble. "The Important New Drug Target in Cardiovascular Medicine – the Vascular Glycocalyx." Cardiovascular & Hematological Disorders-Drug Targets, 2009, 9, p. 118-123
  8. ↑ Van de Berg, Bernard M., Max Nieuwdorp, Erik S.G. Stroes, Hans Vink. Glycocalyx and endothelial (dys) function: from mice to men. Pharmacological Reports, 2006, 57: 75-80.
  9. ↑ Reitsma, Sietze; Slaaf, Dick W.; Vink, Hans; van Zandvoort, Marc A. M. J.; oude Egbrink, Mirjam G. A. (June 2007). "The endothelial glycocalyx: composition, functions, and visualization". Pflügers Archiv: European Journal of Physiology. 454 (3): 345–359. doi:10.1007/s00424-007-0212-8. PMC   1915585 . PMID   17256154.
  10. ↑ Drake-Holland, Angela & Mark Noble. "The Important New Drug Target in Cardiovascular Medicine – the Vascular Glycocalyx." Cardiovascular & Hematological Disorders-Drug Targets, 2009, 9, p. 118–123
  11. ↑ Annecke, T., et al. "Shedding of the coronary endothelial glycocalyx: effects of hypoxia/reoxygenation vs ischaemia/reperfusion." British Journal of Anaesthesia, 2011. 107 (5): 679–86
  12. ↑ Henry, Charmaine B. S.; Duling, Brian R. (2000-12-01). "TNF-α increases entry of macromolecules into luminal endothelial cell glycocalyx". American Journal of Physiology. Heart and Circulatory Physiology. 279 (6): H2815–H2823. doi: 10.1152/ajpheart.2000.279.6.H2815 . ISSN   0363-6135. PMID   11087236. S2CID   86646327.
  13. ↑ Zuurbier, Coert J.; Demirci, Cihan; Koeman, Anneke; Vink, Hans; Ince, Can (October 2005). "Short-term hyperglycemia increases endothelial glycocalyx permeability and acutely decreases lineal density of capillaries with flowing red blood cells". Journal of Applied Physiology. 99 (4): 1471–1476. doi:10.1152/japplphysiol.00436.2005. ISSN   8750-7587. PMID   16024521.
  14. ↑ Mulivor, A. W.; Lipowsky, H. H. (May 2004). "Inflammation- and ischemia-induced shedding of venular glycocalyx". American Journal of Physiology. Heart and Circulatory Physiology. 286 (5): H1672–H1680. doi:10.1152/ajpheart.00832.2003. ISSN   0363-6135. PMID   14704229.
  15. ↑ Becker, Bernhard F.; Jacob, Matthias; Leipert, Stephanie; Salmon, Andrew H. J.; Chappell, Daniel (September 2015). "Degradation of the endothelial glycocalyx in clinical settings: searching for the sheddases: Endothelial glycocalyx - emerging clinical impact". British Journal of Clinical Pharmacology. 80 (3): 389–402. doi:10.1111/bcp.12629. PMC   4574825 . PMID   25778676.
  16. ↑ Steppan, Jochen; Hofer, Stefan; Funke, Benjamin; Brenner, Thorsten; Henrich, Michael; Martin, Eike; Weitz, Jürgen; Hofmann, Ursula; Weigand, Markus A. (January 2011). "Sepsis and major abdominal surgery lead to flaking of the endothelial glycocalix". The Journal of Surgical Research. 165 (1): 136–141. doi:10.1016/j.jss.2009.04.034. ISSN   1095-8673. PMID   19560161.
  17. ↑ Becker, Bernhard F.; Jacob, Matthias; Leipert, Stephanie; Salmon, Andrew H. J.; Chappell, Daniel (September 2015). "Degradation of the endothelial glycocalyx in clinical settings: searching for the sheddases". British Journal of Clinical Pharmacology. 80 (3): 389–402. doi:10.1111/bcp.12629. ISSN   1365-2125. PMC   4574825 . PMID   25778676.
  18. ↑ van der Heijden, Jaap; Kolliopoulos, Constantinos; Skorup, Paul; Sallisalmi, Marko; Heldin, Paraskevi; Hultström, Michael; Tenhunen, Jyrki (2021-10-11). "Plasma hyaluronan, hyaluronidase activity and endogenous hyaluronidase inhibition in sepsis: an experimental and clinical cohort study". Intensive Care Medicine Experimental. 9 (1): 53. doi: 10.1186/s40635-021-00418-3 . ISSN   2197-425X. PMC   8502523 . PMID   34632531.
  19. ↑ Gouverneur, Mirella. Dissertation. "Fluid shear stress directly stimulates synthesis of the endothelial glycocalyx : perturbations by hyperglycemia." 2006. University of Amsterdam. p. 115–153
  20. ↑ Costerton & Irvin. Bacterial Glycocalyx in Nature and Disease. Annual Reviews Microbiology, 1981. Vol. 35: p. 299-324
  21. ↑ Near-Wall {micro}-PIV Reveals a Hydrodynamically Relevant Endothelial Surface Layer in Venules In Vivo - Smith et al. 85 (1): 637 - Biophysical Journal Archived 2008-12-03 at the Wayback Machine
  22. ↑ Schroter, Sabine; Osterhoff, Caroline; McArdle, Wendy; Ivell, Richard (1999). "The glycocalyx of the sperm surface". Human Reproduction Update. 5 (4): 302–313. doi: 10.1093/humupd/5.4.302 . PMID   10465522.
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