Cellular communication (biology)

Cellular communication is an umbrella term used in biology and more in depth in biophysics, biochemistry and biosemiotics to identify different types of communication methods between living cellulites. Some of the methods include cell signaling among others. This process allows millions of cells to communicate and work together to perform important bodily processes that are necessary for survival. Both multicellular and unicellular organisms heavily rely on cell-cell communication.[1]

Intercellular communication

Intercellular communication refers to the communication between cells. Membrane vesicle trafficking has an important role in intercellular communications in humans and animals, e.g., in synaptic transmission, hormone secretion via vesicular exocytosis. Inter-species and interkingdom signaling is the latest field of research for microbe-microbe and microbe-animal/plant interactions for variety of purposes at the host-pathogen interface.

Three stages of cell communication

Reception
A G Protein-coupled receptor within the plasma membrane.

Reception occurs when the target cell (any cell with a receptor protein specific to the signal molecule) detects a signal, usually in the form of a small, water-soluble molecule, via binding to a receptor protein. Reception is the target cell's detection of a signal via binding of a signaling molecule, or ligand. Receptor proteins span the cell’s plasma membrane and provide specific sites for water-soluble signaling molecules to bind to. These trans-membrane receptors are able to transmit information from outside the cell to the inside because they change conformation when a specific ligand binds to it. By looking at three major types of receptors, (G protein coupled receptors, receptor tyrosine kinases, and ion channel receptors) scientists are able to see how trans-membrane receptors contribute to the complexity of cells and the work that these cells do. Cell surface receptors play an essential role in the biological systems of single- and multi-cellular organisms and malfunction or damage to these proteins is associated with cancer, heart disease, and asthma.[2]

Transduction

When binding to the signaling molecule, the receptor protein changes in some way and starts the process of transduction. A specific cellular response is the result of the newly converted signal. Usually, transduction requires a series of changes in a sequence of different molecules (called a signal transduction pathway) but sometimes can occur in a single step. The molecules that compose these pathways are known as relay molecules. The multistep process of the transduction stage is often composed of the activation of proteins by addition or removal of phosphate groups or even the release of other small molecules or ions that can act as messengers. The amplifying of a signal is one of the benefits to this multiple step sequence. Other benefits include more opportunities for regulation than simpler systems do and the fine- tuning of the response, in both unicellular and multicellular organism.[3]

Response

A specific cellular response is the result of the transduced signal in the final stage of cell signaling. This response can essentially be any cellular activity that is present in a body. It can spur the rearrangement of the cytoskeleton, or even as catalysis by an enzyme. These three steps of cell signaling all ensure that the right cells are behaving as told, at the right time, and in synchronization with other cells and their own functions within the organism. At the end, the end of a signal pathway leads to the regulation of a cellular activity. This response can take place in the nucleus or in the cytoplasm of the cell. A majority of signaling pathways control protein synthesis by turning certain genes on and off in the nucleus. [4]

Local and long distance signaling

Local

Communicating through direct contact is one form of local signaling for eukaryotic cells. Plant and animal cells possess junctions that connect the cytoplasm of cells adjacent to one another. These connections allow for signaling substances that were dissolved in the cytosol to easily pass between the cells that are connected. Animal cells contain gap junctions and can communicate through these junctions in a process called cell–cell recognition. Plant cells are connected through plasmodesmata. Embryonic development and the immune response rely heavily on this type of local signaling. In other types of local signaling, the signaling cell secretes messenger molecules that only travel short distances. These local regulators influence cells in the vicinity and can stimulate nearby target cells to perform an action. A number of cells can receive messages and respond to another molecule within their vicinity at the same time. This process of local signaling within animal cells is known as paracrine signaling.

Long distance

Hormones are used by both plant and animal cells for long-distance signaling. In animal cells, specialized cells release these hormones and send them through the circulatory system to other parts of the body. They then reach target cells, which can recognize and respond to the hormones and produce a result. This is also known as endocrine signaling. Plant growth regulators, or plant hormones, move through cells or by diffusing through the air as a gas to reach their targets.[3]

Cell signaling and impacts

There are three different tpes of basic cell communication: surface membrane to surface membrane; exterior, which is between receptors on the cell; and direct communication, which means signals pass inside the cell itself. The junctions of these cells are important because they are the means by which cells communicate with one another. Epithelial cells especially rely on these junctions because when one is injured, these junctions provide the means and communication to seal these injuries. These junctions are especially present in the organs of most species.[5] However, it is also through cell signaling that tumors and cancer can also develop. Stem cells and tumor-causing cells, however, do not have gap junctions so they cannot be affected in the way that one would control a typical epithelial cell.[6] Upstream cells signaling pathways control the proteins and genes that are expressed, which can both create a means for cancer to develop without stopping or a means for treatment for these diseases by targeting these specific upstream signaling pathways.[7] Much of cell communication happens when ligands bind to the receptors of the cell membrane and control the actions of the cell through this binding.[8] Genes can be suppressed, they can be over expressed, or they can be partially inhibited through cell signaling transduction pathways. Some research has found that when gap junction genes were transfected into tumor cells that did not have the gap junction genes, the tumor cells became stable and points to the ability of gap junction genes to inhibit tumors.[6] This stability leads researchers to believe that gap junctions will be a part of cancer treatment in the future.

Communication in cancer

cells will often communicate via gap junctions, which are proteins known as connexins. These connexins have been shown to suppress cancer cells, but this suppression is not the only thing that connexins facilitates. Connexins can also promote tumor progression; therefore, this makes connexins only conditional tumor suppressors.[5] However, this relationship that connects cells makes the spreading of drugs through a system much more effective as small molecules can pass through gap junctions and spread the drug much more quickly and efficiently.[9] The idea that increasing cell communication, or more specifically, connexins, to suppress tumors has been a long, ongoing debate[10] that is supported by the fact that so many types of cancer, including liver cancer, lack the cell communication that characterizes normal cells.

See also

References
  1. Reece JB (September 27, 2010). Campbell Biology (9 ed.). Benjamin Cummings. p. 205. ISBN 978-0-321-55823-7.
  2. Han R, Bansal D, Miyake K, Muniz VP, Weiss RM, McNeil PL, Campbell KP (July 2007). "Dysferlin-mediated membrane repair protects the heart from stress-induced left ventricular injury". The Journal of Clinical Investigation. 117 (7): 1805–13. doi:10.1172/JCI30848. PMC 1904311. PMID 17607357. Lay summary – Science Daily.
  3. Reece JB (Sep 27, 2010). Campbell Biology. Benjamin Cummings. p. 214. ISBN 978-0321558237.
  4. Reece JB (Sep 27, 2010). Campbell Biology (9th ed.). Benjamin Cummings. p. 215. ISBN 978-0-321-55823-7.
  5. Loewenstein WR (February 1972). "Cellular communication through membrane junctions. Special consideration of wound healing and cancer". Archives of Internal Medicine. 129 (2): 299–305. doi:10.1001/archinte.1972.00320020143012. PMID 4333645.
  6. Signal Transduction and Communication in Cancer Cells. The New York Academy of Sciences. 2004. ISBN 978-1-57331-559-3.
  7. Lu KP (April 2004). "Pinning down cell signaling, cancer and Alzheimer's disease". Trends in Biochemical Sciences. 29 (4): 200–9. doi:10.1016/j.tibs.2004.02.002. PMID 15082314.
  8. Schlessinger J (October 2000). "Cell signaling by receptor tyrosine kinases". Cell. 103 (2): 211–25. doi:10.1016/S0092-8674(00)00114-8. PMID 11057895. S2CID 11465988.
  9. Naus CC, Laird DW (June 2010). "Implications and challenges of connexin connections to cancer". Nature Reviews. Cancer. 10 (6): 435–41. doi:10.1038/nrc2841. PMID 20495577. S2CID 28485061.
  10. Loewenstein WR, Kanno Y (March 1966). "Intercellular communication and the control of tissue growth: lack of communication between cancer cells". Nature. 209 (5029): 1248–9. Bibcode:1966Natur.209.1248L. doi:10.1038/2091248a0. PMID 5956321. S2CID 4148588.

Further reading
  • Li J, Habbes HW, Eiberger J, Willecke K, Dermietzel R, Meier C (January 2007). "Analysis of connexin expression during mouse Schwann cell development identifies connexin29 as a novel marker for the transition of neural crest to precursor cells". Glia. 55 (1): 93–103. doi:10.1002/glia.20427. PMID 17024657.
  • Melke P, Jönsson H, Pardali E, ten Dijke P, Peterson C (December 2006). "A rate equation approach to elucidate the kinetics and robustness of the TGF-beta pathway". Biophysical Journal. 91 (12): 4368–80. Bibcode:2006BpJ....91.4368M. doi:10.1529/biophysj.105.080408. PMC 1779910. PMID 17012329.
  • Ishimura A, Ng JK, Taira M, Young SG, Osada S (October 2006). "Man1, an inner nuclear membrane protein, regulates vascular remodeling by modulating transforming growth factor beta signaling". Development (Cambridge, England). 133 (19): 3919–28. doi:10.1242/dev.02538. PMID 16943282. S2CID 21917844.
  • Bell RL, Kimpel MW, Rodd ZA, Strother WN, Bai F, Peper CL, Mayfield RD, Lumeng L, Crabb DW, McBride WJ, Witzmann FA (August 2006). "Protein expression changes in the nucleus accumbens and amygdala of inbred alcohol-preferring rats given either continuous or scheduled access to ethanol". Alcohol. Fayetteville, N.Y. 40 (1): 3–17. doi:10.1016/j.alcohol.2006.10.001. PMID 17157716.
  • Bradshaw R, Dennis E, eds. (2009). Handbook of Cell Signaling. Academic Press. ISBN 978-0-12-374145-5.
  • Cox RP (1974). Cell communication. New York: Wiley. ISBN 0-471-18135-8.
  • Rasmussen H, ed. (1991). "Cell communication in health and disease". Readings from Scientific American Magazine. WH Freeman. ISBN 0-7167-2224-0.
  • Gundelfinger ED, Seidenbecher CI, Schraven B, eds. (2006). Cell communication in nervous and immune system (1st ed.). New York: Springer. ISBN 3-540-36828-0.
  • "Cell Adhesion & Communication". Cell Communication & Adhesion. Yverdon, Switzerland ; New York: Harwood Academic Publishers. 7 (6). May 1993. ISSN 1061-5385.
  • Cell Communication & Adhesion. 8. Basingstoke, Hants, UK: Harwood Academic Publishers. 2001. ISSN 1541-9061.
  • Friedman M, Friedman B (2005). Cell communication : understanding how information is stored and used in cells (1st ed.). New York: Rosen Pub. Group. ISBN 1-4042-0319-2.
  • Bukauskas F, ed. (1991). Intercellular communication. Manchester: Manchester University Press. ISBN 0-7190-3269-5.
  • De Mello WC, ed. (1977). Intercellular communication. New York: Plenum Press. ISBN 0-306-30958-0.
  • Parker JW, O'Brien RL, eds. (December 1982). Intercellular communication in leucocyte function. proceedings of the 15th International Leucocyte Culture Conference, Asilomar and Pacific Grove, Calif. (15th ed.). Chichester ; New York: Wiley. ISBN 0-471-90161-X.
  • Fleming AJ, ed. (2005). Intercellular communication in plants. Oxford: Blackwell. ISBN 1-4051-2068-1.
  • Gunning BE, Robards AW, eds. (1976). Intercellular communication in plants : studies on plasmodesmata. Berlin ; New York: Springer-Verlag. ISBN 0-387-07570-4.
  • Kanno Y, et al., eds. (1995). Intercellular communication through gap junctions. Amsterdam ; New York: Elsevier. ISBN 0-444-81929-0.
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