Cellular adhesion

Cellular adhesion

The process whereby cells interact and attach to other cells or to inanimate surfaces, mediated by interactions between the molecules on the surface of the cell. This process has been studied extensively in embryonic cells of higher organisms, where species and tissue specificity of adhesion has been shown. However, adhesion is a common feature in the life of most organisms.

Prokaryotic microorganisms do not frequently exhibit cell-to-cell interactions, but adhere to surfaces forming biofilms. In these interactions with a surface, some microorganisms cause corrosion of metal by adhering and producing corrosive acid by-products as a result of their metabolism. Adhesion of microorganisms to the cells of higher plants and animals is often a prerequisite for causing disease. Eukaryotic microorganisms often exhibit specific cell-to-cell interactions, allowing complex colonial forms and multicellular organisms to be constructed from individual or free-living cells. Adhesion between different plant cells is apparent in several cases, as in the interaction between a pollen grain and the stigma during fertilization.

Interactions between two cell surfaces may be quite specific, involving certain types of cell-surface protein molecules, or general, involving production of a sticky extracellular matrix that surrounds the cell, as frequently occurs in bacterial adhesion. Cellular adhesion is important in cellular recognition, in the generation of form or pattern, and possibly in regulation of cellular differentiation. See Cell (biology), Cell differentiation

All adhesion is mediated by the cell surface, either directly involving integral components of the plasma membrane, or indirectly through material excreted and deposited on the outside of the cell. Most theories of cellular adhesion suggest that cell-surface glycoproteins serve as ligands involved in attaching cell surfaces together. When a specific cell interacts with an identical cell, the attachment is said to be homotypic. Heterotypic adhesion involves interactions between different cell types. If the ligand-specific attachment involves interaction between identical cell-surface ligands, it is homophilic, and between two different ligands, heterophilic. The interaction between a pollen grain and the stigma cells described previously is an example of a heterotypic, heterophilic interaction.

Many studies of species and tissue specificity have been done with embryonic chick and mouse systems. In general, it would seem that homotypic adhesion is stronger that heterotypic adhesion. Also, tissue and species specific adhesion can be shown, but tissue specificity seems to be more frequent. For example, when dissociated embryonic neural retina of mouse and chick are mixed and allowed to aggregate, there is very little sorting, and mosaic tissue is formed. This is not true in all tissues, as heart and liver tissue show much greater species specificity than neural retina.

Throughout development, it is necessary for specific adhesion among cells to establish and maintain form. It is also important during development that cells change position, as occurs during gastrulation, or migrate, as with neural crest cells that move from the neural tube to various positions, forming ganglia. In these cases, it would seem to be necessary for certain cells to dissociate or alter their adhesive properties in response to the proper developmental cues. Throughout development, there are a series of primary and secondary inductions that affect cellular differentiation and pattern formation. These inductions depend on interactions between cell types having different histories, either due to being in different embryonic layers or due to interaction between cells derived from the same layer but previously differentiated. These changes in form are related to specific changes in cell-adhesion molecules.

References in periodicals archive ?
The role of the cytoskeleton in cellular adhesion molecule expression in tumor necrosis factor-stimulated endothelial cells.
Cellular adhesion molecules play an important role in the process of peritoneal adhesion formation.
Endothelium is a key regulator of vascular homeo-stasis and responds to physical and chemical stimuli by producing factors that regulate vascular tone, cellular adhesion, thromboresistance, smooth muscle cell (SMC) proliferation, and vessel wall inflammation.
However, cellular adhesion shows a decrease over time, which is a positive outcome for catheter use since catheters during radiotherapy are temporary implants, and therefore, decreased cell adhesion is preferred.
Patterned surfaces may have a potential interest in medicine and dentistry for enhancing the surface of devices such as orthopedic implants, dental prosthetics, cardiac valves, or osseous-fixation plates, among others, as modified surfaces have demonstrated not only a reduction in bacterial adhesion [3-6] but also an improvement in cellular adhesion and arrangement [10, 11], which will ultimately lead to improving the correlation between biomaterials/devices and surrounding tissues.
The biomaterial should be both biocompatible and biodegradable, and able to support cellular adhesion and proliferation (11).
Defactinib (VS-6063) is an investigational inhibitor of FAK, a non-receptor tyrosine kinase encoded by the PTK-2 gene that mediates oncogenic signaling in response to cellular adhesion and growth factors.
The ED biomarkers include: intercellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), P- and E-selectin, vascular endothelial growth factor (VEGF) and C-reactive protein (CRP) [4].
The extracellular domains of the CEACAM group function as homophilic and heterophilic cellular adhesion molecules or receptors [32-34].
This TM4SF5-mediated activation process appears to involve a conformational release in FAK upon cellular adhesion.
Cellular adhesion molecules like iutracellular adhesion molecule (ICAM) and Vascular cell adhesion molecules-1 (VCAM-1) can be considered potential markers of vulnerability because such molecules are activated by inflammatory cytokines and chemokines and then released by the endothelium.

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