La adhesión celular es el proceso mediante el cual las células interactúan y se adhieren a las células vecinas a través de moléculas especializadas de la superficie celular. Este proceso puede ocurrir a través del contacto directo entre las superficies celulares, como las uniones celulares, o la interacción indirecta, donde las células se adhieren a la matriz extracelular circundante , una estructura similar a un gel que contiene moléculas liberadas por las células en los espacios entre ellas. [1] La adhesión celular se produce a partir de interacciones entre moléculas de adhesión celular (CAM), [2] proteínas transmembrana ubicadas en la superficie celular. La adhesión celular une las células de diferentes maneras y puede estar involucrada en la transducción de señales.para que las células detecten y respondan a cambios en el entorno. [1] [3] Otros procesos celulares regulados por la adhesión celular incluyen la migración celular y el desarrollo de tejidos en organismos multicelulares . [4] Las alteraciones en la adhesión celular pueden alterar importantes procesos celulares y conducir a una variedad de enfermedades, incluyendo cáncer [5] [6] y artritis . [7] La adhesión celular también es esencial para que los organismos infecciosos, como bacterias o virus , causen enfermedades . [8] [9]
Mecanismo general
Las CAM se clasifican en cuatro familias principales: integrinas , superfamilia de inmunoglobulinas (Ig) , cadherinas y selectinas . [2] Las cadherinas y las IgSF son CAM homófilas, ya que se unen directamente al mismo tipo de CAM en otra célula, mientras que las integrinas y las selectinas son CAM heterófilas que se unen a diferentes tipos de CAM. [2] [ cita requerida ] Cada una de estas moléculas de adhesión tiene una función diferente y reconoce diferentes ligandos . Los defectos en la adhesión celular suelen atribuirse a defectos en la expresión de CAM.
En los organismos multicelulares, las uniones entre las CAM permiten que las células se adhieran entre sí y crean estructuras llamadas uniones celulares . Según sus funciones, las uniones celulares se pueden clasificar como: [1]
- Uniones de anclaje (uniones adheridas , desmosomas y hemidesmosomas ), que mantienen unidas las células y fortalecen el contacto entre células.
- Oclusiones (uniones estrechas ), que sellan los espacios entre las células a través del contacto célula-célula, creando una barrera impermeable para la difusión.
- Uniones formadoras de canales (uniones gap ), que enlazan el citoplasma de las células adyacentes, lo que permite que se produzca el transporte de moléculas entre las células.
- Uniones de retransmisión de señales, que pueden ser sinapsis en el sistema nervioso.
Alternativamente, las uniones celulares se pueden clasificar en dos tipos principales de acuerdo con lo que interactúa con la célula: las uniones célula-célula, principalmente mediadas por cadherinas, y las uniones célula-matriz, principalmente mediadas por integrinas.
Uniones celda-celda
Las uniones célula-célula pueden ocurrir de diferentes formas. Al anclar uniones entre células, como uniones adherentes y desmosomas, las principales CAM presentes son las cadherinas. Esta familia de CAM son proteínas de membrana que median la adhesión célula-célula a través de sus dominios extracelulares y requieren iones de Ca 2+ extracelulares para funcionar correctamente. [2] Las cadherinas forman una unión homofílica entre sí, lo que da como resultado que las células de un tipo similar se unan y pueden conducir a una adhesión celular selectiva, lo que permite que las células de los vertebrados se reúnan en tejidos organizados. [1] Las cadherinas son esenciales para la adhesión célula-célula y la señalización celular en animales multicelulares y se pueden separar en dos tipos: cadherinas clásicas y cadherinas no clásicas. [2]
Adherens junctions
Adherens junctions mainly function to maintain the shape of tissues and to hold cells together. In adherens junctions, cadherins between neighbouring cells interact through their extracellular domains, which share a conserved calcium-sensitive region in their extracellular domains. When this region comes into contact with Ca2+ ions, extracellular domains of cadherins undergo a conformational change from the inactive flexible conformation to a more rigid conformation in order to undergo homophilic binding. Intracellular domains of cadherins are also highly conserved, as they bind to proteins called catenins, forming catenin-cadherin complexes. These protein complexes link cadherins to actin filaments. This association with actin filaments is essential for adherens junctions to stabilise cell–cell adhesion.[10][11][12] Interactions with actin filaments can also promote clustering of cadherins, which are involved in the assembly of adherens junctions. This is since cadherin clusters promote actin filament polymerisation ,which in turn promotes the assembly of adherens junctions by binding to the cadherin–catenin complexes that then form at the junction.[citation needed]
Desmosomes
Desmosomes are structurally similar to adherens junctions but composed of different components. Instead of classical cadherins, non-classical cadherins such as desmogleins and desmocollins act as adhesion molecules and they are linked to intermediate filaments instead of actin filaments.[13] No catenin is present in desmosomes as intracellular domains of desmosomal cadherins interact with desmosomal plaque proteins, which form the thick cytoplasmic plaques in desmosomes and link cadherins to intermediate filaments.[14] Desmosomes provides strength and resistance to mechanical stress by unloading forces onto the flexible but resilient intermediate filaments, something that cannot occur with the rigid actin filaments.[13] This makes desmosomes important in tissues that encounter high levels of mechanical stress, such as heart muscle and epithelia, and explains why it appears frequently in these types of tissues.
Tight junctions
Tight junctions are normally present in epithelial and endothelial tissues, where they seal gaps and regulate paracellular transport of solutes and extracellular fluids in these tissues that function as barriers.[15] Tight junction is formed by transmembrane proteins, including claudins, occludins and tricellulins, that bind closely to each other on adjacent membranes in a homophilic manner.[1] Similar to anchoring junctions, intracellular domains of these tight junction proteins are bound with scaffold proteins that keep these proteins in clusters and link them to actin filaments in order to maintain structure of the tight junction.[16] Claudins, essential for formation of tight junctions, form paracellular pores which allow selective passage of specific ions across tight junctions making the barrier selectively permeable.[15]
Gap junctions
Gap junctions are composed of channels called connexons, which consist of transmembrane proteins called connexins clustered in groups of six.[17] Connexons from adjacent cells form continuous channels when they come into contact and align with each other. These channels allow transport of ions and small molecules between cytoplasm of two adjacent cells, apart from holding cells together and provide structural stability like anchoring junctions or tight junctions.[1] Gap junction channels are selectively permeable to specific ions depending on which connexins form the connexons, which allows gap junctions to be involved in cell signalling by regulating the transfer of molecules involved in signalling cascades.[18] Channels can respond to many different stimuli and are regulated dynamically either by rapid mechanisms, such as voltage gating, or by slow mechanism, such as altering numbers of channels present in gap junctions.[17]
Adhesion mediated by selectins
Selectins are a family of specialised CAMs involved in transient cell–cell adhesion occurring in the circulatory system. They mainly mediate the movement of white blood cells (leukocytes) in the bloodstream by allowing the white blood cells to "roll" on endothelial cells through reversible bindings of selections.[19] Selectins undergo heterophilic bindings, as its extracellular domain binds to carbohydrates on adjacent cells instead of other selectins, while it also require Ca2+ ions to function, same as cadherins.[1] cell–cell adhesion of leukocytes to endothelial cells is important for immune responses as leukocytes can travel to sites of infection or injury through this mechanism.[20] At these sites, integrins on the rolling white blood cells are activated and bind firmly to the local endothelial cells, allowing the leukocytes to stop migrating and move across the endothelial barrier.[20]
Adhesion mediated by members of the immunoglobulin superfamily
The immunoglobulin superfamily (IgSF) is one of the largest superfamily of proteins in the body and it contains many diverse CAMs involved in different functions. These transmembrane proteins have one or more immunoglobulin-like domains in their extracellular domains and undergo calcium-independent binding with ligands on adjacent cells.[21] Some IgSF CAMs, such as neural cell adhesion molecules (NCAMs), can perform homophilic binding while others, such as intercellular cell adhesion molecules (ICAMs) or vascular cell adhesion molecules (VCAMs) undergo heterophilic binding with molecules like carbohydrates or integrins.[22] Both ICAMs and VCAMs are expressed on vascular endothelial cells and they interact with integrins on the leukocytes to assist leukocyte attachment and its movement across the endothelial barrier.[22]
Cell–matrix junctions
Cells create extracellular matrix by releasing molecules into its surrounding extracellular space. Cells have specific CAMs that will bind to molecules in the extracellular matrix and link the matrix to the intracellular cytoskeleton.[1] Extracellular matrix can act as a support when organising cells into tissues and can also be involved in cell signalling by activating intracellular pathways when bound to the CAMs.[2] Cell–matrix junctions are mainly mediated by integrins, which also clusters like cadherins to form firm adhesions. Integrins are transmembrane heterodimers formed by different α and β subunits, both subunits with different domain structures.[23] Integrins can signal in both directions: inside-out signalling, intracellular signals modifying the intracellular domains, can regulate affinity of integrins for their ligands, while outside-in signalling, extracellular ligands binding to extracellular domains, can induce conformational changes in integrins and initiate signalling cascades.[23] Extracellular domains of integrins can bind to different ligands through heterophilic binding while intracellular domains can either be linked to intermediate filaments, forming hemidesmosomes, or to actin filaments, forming focal adhesions.[24]
Hemidesmosomes
In hemidesmosomes, integrins attach to extracellular matrix proteins called laminins in the basal lamina, which is the extracellular matrix secreted by epithelial cells.[1] Integrins link extracellular matrix to keratin intermediate filaments, which interacts with intracellular domain of integrins via adapter proteins such as plectins and BP230.[25] Hemidesmosomes are important in maintaining structural stability of epithelial cells by anchoring them together indirectly through the extracellular matrix.
Focal adhesions
In focal adhesions, integrins attach fibronectins, a component in the extracellular matrix, to actin filaments inside cells.[24] Adapter proteins, such as talins, vinculins, α-actinins and filamins, form a complex at the intracellular domain of integrins and bind to actin filaments.[26] This multi-protein complex linking integrins to actin filaments is important for assembly of signalling complexes that act as signals for cell growth and cell motility.[26]
Otros organismos
Eukaryotes
Plants cells adhere closely to each other and are connected through plasmodesmata, channels that cross the plant cell walls and connect cytoplasms of adjacent plant cells.[27] Molecules that are either nutrients or signals required for growth are transported, either passively or selectively, between plant cells through plasmodesmata.[27]
Protozoans express multiple adhesion molecules with different specificities that bind to carbohydrates located on surfaces of their host cells.[28] cell–cell adhesion is key for pathogenic protozoans to attach en enter their host cells. 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,[29] and another adhesion molecule called the merozoite surface protein to bind red blood cells.[30]
Pathogenic fungi use adhesion molecules present on its cell wall to attach, either through protein-protein or protein-carbohydrate interactions, to host cells[31] or fibronectins in the extracellular matrix.[32]
Prokaryotes
Prokaryotes have adhesion molecules on their cell surface termed bacterial adhesins, apart from using its pili (fimbriae) and flagella for cell adhesion.[8] Adhesins can recognise a variety of ligands present on the host cell surfaces and also components in the extracellular matrix. These molecules also control host specificity and regulate tropism (tissue- or cell-specific interactions) through their interaction with their ligands.[33]
Viruses
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.[34] HIV has an adhesion molecule termed gp120 that binds to its ligand CD4, which is expressed on lymphocytes.[35] Viruses can also target components of cell junctions to enter host cells, which is what happens when the hepatitis C virus targets occludins and claudins in tight junctions to enter liver cells.[9]
Implicaciones clínicas
Dysfunction of cell adhesion occurs during cancer metastasis. Loss of cell–cell adhesion in metastatic tumour cells allows them to escape their site of origin and spread through the circulatory system.[5] One example of CAMs deregulated in cancer are cadherins, which are inactivated either by genetic mutations or by other oncogenic signalling molecules, allowing cancer cells to migrate and be more invasive.[6] Other CAMs, like selectins and integrins, can facilitate metastasis by mediating cell–cell interactions between migrating metastatic tumour cells in the circulatory system with endothelial cells of other distant tissues.[36] Due to the link between CAMs and cancer metastasis, these molecules could be potential therapeutic targets for cancer treatment.
There are also other human genetic diseases caused by an inability to express specific adhesion molecules. An example is leukocyte adhesion deficiency-I (LAD-I), where expression of the β2 integrin subunit is reduced or lost.[37] This leads to reduced expression of β2 integrin heterodimers, which are required for leukocytes to firmly attach to the endothelial wall at sites of inflammation in order to fight infections.[38] Leukocytes from LAD-I patients are unable to adhere to endothelial cells and patients exhibit serious episodes of infection that can be life-threatening.
An autoimmune disease called pemphigus is also caused by loss of cell adhesion, as it results from autoantibodies targeting a person's own desmosomal cadherins which leads to epidermal cells detaching from each other and causes skin blistering.[39]
Pathogenic microorganisms, including bacteria, viruses and protozoans, have to first adhere to host cells in order to infect and cause diseases. Anti-adhesion therapy can be used to prevent infection by targeting adhesion molecules either on the pathogen or on the host cell.[40] Apart from altering the production of adhesion molecules, competitive inhibitors that bind to adhesion molecules to prevent binding between cells can also be used, acting as anti-adhesive agents.[41]
Ver también
- Cell communication (biology)
- Epithelium
- Cytoskeleton
- Differential adhesion hypothesis
- Role of cell adhesions in neural development
Referencias
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enlaces externos
- The Cell by G. Cooper (online textbook)
- Molecular Cell Biology by Lodish et al. (online textbook)
- Molecular Biology of the Cell by Alberts et al. (online textbook)
- Cell Adhesion and Extracellular Matrix - The Virtual Library of Biochemistry, Molecular Biology and Cell Biology