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L cells expressing P-cadherin adhere to one another, and to other types of cells that express this cadherin. Thus, cadherins directly cause homotypic interactions among cells. The mechanism for cell-cell adhesion is explained by the atomic structures of the N-terminal domains from E- and N- cadherin. The current model proposes that cadherin molecules associate through their N-terminal domains into a parallel homodimer see Figure Furthermore, cell-cell adhesion results from head-to-head contact between cadherin dimers in adjacent cell membranes.

Unlike cadherins, N-CAMs are encoded by a single gene ; their diversity is generated by alternative mRNA splicing and by differences in glycosylation Figure Like N- cadherin , N-CAMs appear during morphogenesis, playing an important role in differentiation of muscle, glial, and nerve cells. Their role in cell adhesion has been directly demonstrated by use of specific antibodies.

For instance, adhesion of cultured retinal neurons is inhibited by addition of antibodies to N-CAMs. The adhesive properties of N- CAMs are modulated by long chains of sialic acid , a negatively charged sugar see Figure N-CAMs that are heavily sialylated form weaker homophilic interactions than do less sialylated forms, possibly because of repulsion between the negatively charged sialic acid residues.

In embryonic tissues such as brain, polysialic acid constitutes as much as 25 percent of the mass of N-CAMs; in contrast, N-CAMs from adult tissues contain only one-third as much sialic acid. The lower adhesive properties of embryonic N-CAMs enable cell-cell contacts to be made and then broken, a property necessary for specific cell contacts to form in the developing nervous system. The higher adhesive properties of the adult forms of N-CAM stabilize these contacts. Thus, the strength of cell-cell adhesions is modified during differentiation by differential glycosylation of the N-CAMs.

Thus far we have considered cell interactions in solid tissues, such as epithelia and neuronal tissue.

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Once these interactions form during differentiation , they generally are stable for the life of the cells. In adult organisms, many types of cells that participate in defense against foreign invaders e. Movement into tissue, termed extravasation, of four types of leukocytes white blood cells is particularly important: Extravasation requires the successive formation and breakage of cell-cell contacts between leukocytes in the blood and endothelial cells lining the vessels. A key protein in this process, P-selectin, is localized to the blood-facing surface of endothelial cells.

Like other members of the selectin family of CAMs, P-selectin is a lectin , a protein that binds to carbohydrates. Each type of selectin binds to specific oligosaccharide sequences in glycoproteins or glycolipids.

The sugar-binding lectin domain in selectins generally is at the end of the extracellular region of the molecule see Figure The ligand for P-selectin is a specific oligosaccharide sequence, called the sialyl Lewis-x antigen , that is part of longer oligosaccharides present in abun-dance on leukocyte glycoproteins and glycolipids. As illustrated in Figure , in normal endothelial cells P-selectin is localized to intracellular vesicles and is not present on the plasma membrane. These cells are activated by various inflammatory signals released by surrounding cells in areas of infection or inflammation.

Cell-Cell Adhesion and Communication - Molecular Cell Biology - NCBI Bookshelf

Once endothelial cells are activated, the vesicles containing P-selectin undergo exocytosis within seconds, and P-selectin appears on the plasma membrane. Interactions between cell-adhesion molecules during the initial binding and tight binding of T cells, a kind of leukocyte, to activation endothelial cells. Once a T cell has firmly adhered to the endothelium, it can move extravasate into the underlying more Thus, the selective adhesion of T lymphocytes to the endothelium near sites of infection or inflammation depends on the sequential appearance and activation of several different CAMs on the surface of the interacting cells.

Although hundreds of individual cell-cell adhesions are sufficient to cause cells to adhere, specialized junctions consisting of dense clusters of cell-adhesion molecules are required for the function of tissues. Concentrated in this region is E- cadherin , which links the plasma membranes of adjacent cells and via catenin adapter proteins attaches to actin filaments in adherens junctions or keratin filaments in desmosomes Figure Adhesion molecules in junctions involved in cell-cell adhesion.

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Adherens junctions and desmosomes are specialized cell-cell junctions that consist of clustered-cadherin dimers. Cadherin is connected to either the circumferential belt of actin filaments more Epithelial cells contain a continuous band of cadherin molecules, usually located near the apical surface just below the tight junction , that connects the lateral membranes of epithelial cells see Figure As a complex with the adherens junction, the circumferential belt functions as a tension cable that can internally brace the cell and thereby control its shape.

The transmembrane linker proteins, called desmoglein and desmocollin, belong to the cadherin family of cell-adhesion molecules. They bind to plakoglobin and other proteins in the plaques and extend into the intercellular space, where they interact, forming an interlocking network that binds two cells together.

Cell Adhesion and Migration in Skin Disease

The transmembrane linker proteins, desmoglein and desmocollin, belong more Desmoglein was first identified by an unusual but revealing skin disease called pemphigus vulgaris, an autoimmune disease. Patients with autoimmune disorders synthesize antibodies that bind to a normal body protein. In this case, the autoantibodies disrupt adhesion between epithelial cells, causing blisters of the skin and mucous membranes. The predominant autoantibody was shown to be specific for desmoglein, a major protein in the skin desmosomes ; indeed, addition of such antibodies to normal skin induces formation of blisters and disruption of cell adhesion.

In epithelial cells, keratin intermediate filaments course near the cytoplasmic plaques of desmosomes and apparently are linked to them by the desmoplakin proteins. Some of these filaments run parallel to the cell surface, and others penetrate and traverse the cytoplasm. They are thought to be part of the internal structural framework of the cell, giving it shape and rigidity. If so, desmosomes also could transmit shearing forces from one region of a cell layer to the epithelium as a whole; they thus provide strength and rigidity to the entire epithelial cell layer. Early electron micrographs showed that almost all animal cells that come in contact with each other have regions of junctional specialization characterized by an intercellular gap, which is filled by a well-defined set of cylindrical particles Figure Morphologists named these regions gap junctions , but in retrospect the gap is not their most important feature.

The cylindrical particles, which are water-filled channels, are the key to the function of gap junctions. These channels directly link the cytosol of one cell with that of an adjacent cell, providing a passageway for movement of very small molecules and ions between the cells. Electron micrograph of a thin section through a gap junction connecting two mouse liver cells. The size of these intercellular channels can be measured by injecting a cell with a fluorescent dye covalently linked to molecules of various sizes and using a fluorescence microscope to observe whether they pass into neighboring cells.

Gap junctions between mammalian cells permit the passage of molecules as large as 1.

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In insects, these junctions are permeable to molecules as large as 2 nm in diameter. Generally speaking, molecules with a molecular weight less than pass freely, and those with a molecular greater than do not pass; the passage of intermediate-sized molecules is variable and limited. Thus ions and many low-molecular-weight building blocks of cellular macromolecules, such as amino acids and nucleoside phosphates, can pass from cell to cell.

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A vivid example of this cell-cell transfer is the phenomenon of metabolic coupling, or metabolic cooperation, in which a cell transfers molecules to a neighboring cell that is unable to synthesize them. This phenomenon can be demonstrated with mutant cells unable to synthesize dATP, an immediate precursor of DNA , from hypoxanthine via a nucleotide -salvage pathway see Figure When cultured alone, these cells cannot incorporate radioactivity from hypoxanthine into their DNA.

However, when the mutant cells are co-cultured with wild-type cells, radioactivity is frequently found in the nuclear DNA of the mutant cells. The mutant and wild-type cells can be differentiated by their distinct morphologies or by feeding one of the cell lines carbon particles before mixing it with the other line.

The dATP derived from hypoxanthine is incorporated only into the DNA of mutant cells that are in direct or indirect contact through an intermediate cell with wild-type cells. It is thought that labeled adenosine mono-, di-, or triphosphate is synthesized from the labeled hypoxanthine by wild-type cells and then passed through gap junctions to the mutant cells.

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  • Another important compound transferred from cell to cell through gap junctions is cyclic AMP cAMP , which acts as an intracellular second messenger. As discussed in Chapter 20, the amount of cellular cAMP increases in response to stimulation of cells by binding of many different hormones. The fact that cAMP can pass through gap junctions means that the hormonal stimulation of just one or a few cells in an epithelium initiates a metabolic reaction in many of them. Thus cells may modulate the degree of coupling with their neighbors, but precisely why and how they accomplish this is a matter of debate.

    In the liver and many other tissues, large numbers of individual gap junction channels cluster together in an area about 0. This property has enabled researchers to separate gap junctions from other components of the plasma membrane by shearing the purified plasma membrane into small fragments. Owing to their relatively high protein content, fragments containing gap junctions have a higher density than the bulk of the plasma membrane and can be purified on an equilibrium density gradient see Figure Electron micrographs of stained, isolated gap junctions reveal a lattice of hexagonal particles with hollow cores as intercellular channels see Figure Leukocytes continually infiltrate the skin and patrol it for potentially harmful pathogens.

    Control of leukocyte adhesion to resident cells within the skin and to the extracellular matrix plays a key role in controlling these processes. These mechanisms constitute the primary focus of the final section. The pivotal role of leukocytes is examined in conjunction with the chronic inflammatory diseases which arise when components of the skin's finely tuned defence strategy go awry and the potential for these anomalies to be pinpointed as important immunotherapeutic targets for skin diseases.

    Table of Contents 1. The Cornified Cell Envelope 3.

    Lymphocyte migration.

    Keratins and Keratin Disorders 4. Biology and Pathology of Hemidesmosomes 8. Leukocyte Trafficking in Skin Diseases Skin Homing Lymphocytes T-cell Accessory Molecules Animal Models of Skin Inflammation Langerhans Cell Migration The Bookshelf application offers access: Offline Computer — Download Bookshelf software to your desktop so you can view your eBooks with or without Internet access.

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