Cellular adhesion is the binding of a cell to a surface, extracellular matrix or another cell using cell adhesion molecules such as selectins, integrins, and cadherins. Correct cellular adhesion is essential in maintaining multicellular structure. Cellular adhesion can link the cytoplasm of cells and can be involved in signal transduction.
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Cell adhesion molecules involved in the process are first hydrolyzed by extracellular enzymes. Cell adhesion is directly related to protein adsorption.
Eukaryotic protozoans express multiple adhesion molecules. An example of a pathogenic protozoan is the malarial parasite (Plasmodium falciparum), which uses one adhesion molecule called the circumsporozoite protein to bind to liver cells, and another adhesion molecule called the merozoite surface protein to bind red blood cells. In human cells, which have many different types of adhesion molecules, the major classes are named integrins, Ig superfamily members, cadherins, and selectins. Each of these adhesion molecules has a different function and recognizes different ligands. Defects in cell adhesion are usually attributable to defects in expression of adhesion molecules.
Cell junctions allow cells to adhere. There are 4 types of cell junctions:[1]
Cell-cell adhesions in Anchoring junctions are mediated by cadherins. Cell–matrix adhesions however, are usually mediated by intergrins.[1]
Selective cell–cell adhesion enables vertebrate cells to assemble into organised tissues. homophilic attachment allows selective recognition resulting. Cells of a similar type stick together where as cells of a different type stay segregated.[1]
Prokaryotes have adhesion molecules usually termed "adhesins". Adhesins may occur on pili (fimbriae), flagellae, or the cell surface. Adhesion of bacteria is the first step in colonization and regulates tropism (tissue- or cell-specific interactions).
Viruses also have adhesion molecules required for viral binding to host cells. For example, influenza virus has a hemagglutinin on its surface that is required for recognition of the sugar sialic acid on host cell surface molecules. HIV has an adhesion molecule termed gp120 that binds to its ligand CD4, which is expressed on lymphocytes.
The differential adhesion hypothesis (sometimes called the "thermodynamic hypothesis")[2] is a theory of cell adhesion advanced by Malcolm Steinberg in 1964 to explain the mechanism by which heterotypic cells in mixed aggregates sort out into isotypic territories. The DAH postulates that tissues are viscoelastic liquids, and as such possess measurable tissue surface tensions. These surface tensions have been determined for a variety of tissues, including embryonic tissues and cell lines. The surface tensions correspond to the mutual sorting behavior: the tissue type with the higher surface tension will occupy an internal position relative to a tissue with a lower surface tension (if these tissues can interact with each other through their adhesion machinery). Quantitative differences in homo and heterotypic adhesion are supposed to be sufficient to account for the phenomenon without the need to postulate cell type specific adhesion systems: fairly generally accepted, although some tissue specific cell adhesion molecules are now known to exist.
Dysfunction of cell-adhesion and cell-migration occurs during cancer metastasis. Cellular adhesion and traction can allow cells to migrate.[1] Cells can form intergrin mediated attachments sites called focal adhesions. Focal adhesions at the leading edge provide the necessary traction allowing the cell to pull its self forward.
Pemphigus is the result of auto-antibodies which target desmosomal cadherins. Results in loss of cell adhesion.
Researchers at Japan's Nagoya University have developed a test to measure the adhesion of a single cell and potentially determine cellular viability.[3]
(1) Gumbiner, B. M. (1996) Cell adhesion: The molecular basis of tissue architecture and morphogenesis. Cell 84, 345-357.
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