Cell–cell interaction

Source: Wikipedia, the free encyclopedia.

Cell–cell interaction refers to the direct interactions between

multicellular
organisms. These interactions allow cells to
cell junctions. These junctions are involved in the communication and organization of cells within a particular tissue. Others are transient or temporary such as those between cells of the immune system or the interactions involved in tissue inflammation. These types of intercellular interactions are distinguished from other types such as those between cells and the extracellular matrix. The loss of communication between cells can result in uncontrollable cell growth and cancer
.

Stable interactions

Various types of cell junctions. In this diagram, the interface between neighboring cells or the basolateral membrane is depicted as "sheets"; the space between these sheets being the extracellular environment and the location of adhesion protein interaction.

Stable cell-cell interactions are required for cell adhesion within a tissue and controlling the shape and function of cells.[1] These stable interactions involve cell junctions which are multiprotein complexes that provide contact between neighboring cells. Cell junctions allow for the preservation and proper functioning of epithelial cell sheets. These junctions are also important in the organization of tissues where cells of one type can only adhere to cells of the same tissue rather than to a different tissue.[2]

Tight junctions

Tight junctions are multi-protein complexes that hold cells of a same tissue together and prevent movement of water and water-soluble molecules between cells. In epithelial cells, they function also to separate the extracellular fluid surrounding their apical and basolateral membranes.[1] These junctions exist as a continuous band located just below the apical surface between the membranes of neighboring epithelial cells. The tight junctions on adjacent cells line up so as to produce a seal between different tissues and body cavities. For example, the apical surface of gastrointestinal epithelial cells serve as a selective permeable barrier that separates the external environment from the body.[3] The permeability of these junctions is dependent on a variety of factors including protein makeup of that junction, tissue type and signaling from the cells.[1]

Tight junctions are made up of many different proteins. The four main transmembrane proteins are occludin, claudin, junctional adhesion molecules (JAMs) and tricellulins. The extracellular domains of these proteins form the tight junction barrier by making homophilic (between proteins of the same kind) and heterophilic interactions (between different types of proteins) with the protein domains on adjacent cells. Their cytoplasmic domains interact with the cell cytoskeleton to anchor them.[3]

Anchoring junctions

Main articles: Cell junction, Desmosome, and Adherens junction

Of the three types of

E-cadherin is the most abundant.[1]

Desmosomes also provide strength and durability to cells and tissues and are located just below adherens junctions. They are sites of adhesion and do not encircle the cell. They are made of two specialized cadherins, desmoglein and desmocollin. These proteins have extracellular domains that interact with each other on adjacent cells. On the cytoplasmic side, plakins form plaques which anchor the desmosomes to intermediate filaments composed of keratin proteins. Desmosomes also play a role in cell-cell signaling.[4]

Gap junctions

vertebrates, gap junctions are composed of transmembrane proteins called connexins. They form hexagonal pores or channels through which ions, sugars, and other small molecules can pass. Each pore is made of 12 connexin molecules; 6 form a hemichannel on one cell membrane and interact with a hemichannel on an adjacent cell membrane. The permeability of these junctions is regulated by many factors including pH and Ca2+ concentration.[1]

Receptor proteins in direct-contact signaling

Main articles:
Signal Transduction and Cell signaling

lipids which project outward and act as signals. Direct contact between cells allows the receptors on one cell to bind the small molecules attached to the plasma membrane of different cell. In eukaryotes, many of the cells during early development communicate through direct contact.[5]

vertebrates, acetylcholine released from the motor neuron acts as a neurotransmitter which depolarizes the muscle fiber and causes muscle contraction. A neuron’s ability to receive and integrate simultaneous signals from the environment and other neurons allows for complex animal behavior.[6]

Plant cell-cell interactions

desmotubule, which spans between the cells. The cell-cell interactions facilitated by plasmodesmata play an important role in development of plant cells and tissues and defense against viral infection.[1]

Transient interactions

Immune system

Main article: Immune system

Leukocytes or white blood cells destroy abnormal cells and also provide protection against bacteria and other foreign matter. These interactions are transitory in nature but are crucial as an immediate immune response. To fight infection, leukocytes must move from the blood into the affected tissues. This movement into tissues is called extravasation. It requires successive forming and breaking of cell-cell interactions between the leukocytes and the endothelial cells that line blood vessels. These cell-cell interactions are mediated mainly by a group of Cell Adhesion Molecules (CAMs) called selectins.[1]

antigens on its surface. T-helper cells that possess the appropriate receptors can bind to these antigens and proliferate resulting in T-helper cells that have the ability to identify the same antigens.[7]

Coagulation

platelets. When the endothelium or the lining of a blood vessel is damaged, connective tissue including collagen fibers is locally exposed. Initially, platelets stick to the exposed connective tissue through specific cell-surface receptors. This is followed by platelet activation and aggregation in which platelets become firmly attached and release chemicals that recruit neighboring platelets to the site of vascular injury. A meshwork of fibrin then forms around this aggregation of platelets to increase the strength of the clot.[8]

Cell interactions between bacteria

Bacterial populations interact in a similar manner to cells in tissue. They communicate through physical interactions and signaling molecules such as homoserine lactones and peptides as a means to control metabolism and regulate growth . A common example and one of the most studied forms of bacterial cell interactions is biofilm. Biofilm is a cell aggregate that can be attached to biological or abiotic surfaces. Bacteria form biofilms to adapt to various environments such as changes in substrate availability. For example, the formation of biofilm increases a bacterial cell's resistance to antibiotics compared to cells which are not part of the aggregate.[9]

Pathological implications

Cancer

Cancer can result from the loss of cell-cell interaction. In normal cells, growth is controlled by contact inhibition in which contact with neighboring cells causes a stunt in cell growth. Contact inhibition is thought to be mediated by cadherins, proteins that play an important role in cell adhesion. This inhibition prevents cells from piling up on top of one another and forming mounds. However, in cancerous cells where expression of E-cadherin is lost, contact inhibition is lost and results in uncontrolled growth or proliferation, tumor formation, and metastasis.[10]

Bacterial pathogens

In order for

toxins into the host cells. These toxins ultimately lead to rearrangement of the cytoskeleton and entry of the bacteria.[11]

Disease

Cell–cell interactions are highly specific and are tightly regulated. Genetic defects and dysregulation of these interactions can cause many different diseases. Dysregulation that leads to leukocyte migration into healthy tissues can cause conditions such as

heart malformations and neurosensory deafness.[1]

References

  1. ^
    ISBN 9780716776017
    .
  2. ISBN 978-0-87893-300-6.{{cite book}}: CS1 maint: multiple names: authors list (link
    )
  3. ^
    S2CID 16512214
    .
  4. PMID 21783027
    .
  5. ISBN 978-0-07-246463-4
    .
  6. PMID 20215342
    .
  7. ISBN 0-8153-4072-9
    .
  8. S2CID 11170987
    .
  9. S2CID 28468434
    .
  10. PMID 20399659
    .
  11. PMID 11393190
    .
  12. S2CID 30311802
    .
Retrieved from "https://en.wikipedia.org/w/index.php?title=Cell–cell_interaction&oldid=1204105325"