The mystery of membrane organization: composition, regulation and roles of lipid rafts. Eukaryotic cells have been confronted throughout their evolution with potentially lethal plasma membrane injuries, including those caused by osmotic stress, by infection from bacterial toxins and parasites, and by mechanical and ischemic stress. Local oxidation at the site of membrane injury activates MG53 oligomerization (Cai et al., 2009), which may locally increase membrane rigidity. Instead, distinct inter- and intra-leaflet heterogeneity exists. Drescher DG, Drescher MJ, Selvakumar D, Annam NP. Shear stress on the plasma membrane also results in the dissociation of the negative regulator RhoGDI and its binding partner Rho (Shao et al., 2018). doi: 10.1016/j.cub.2017.12.034. Bethesda, MD 20894, Web Policies Prior to increase in shear force, PLD associates with lipid rafts, physically segregated from its activator PIP2 and its substrate PC (Petersen et al., 2016). Skalman LN, Holst MR, Larsson E, & Lundmark R (2018). The primary method for PIP2 formation in cells is by the activity of PI(4)P-5 kinase (PI5K) (Kolay, Basu, & Raghu, 2016). Lysosome fusion is required for the process of repair (Reddy, Caler, & Andrews, 2001). Physico-chemical and biological considerations for membrane wound evolution and repair in animal cells. This helps to remodel the newly repaired plasma membrane (Middel et al., 2016), but may also serve to potentiate tissue inflammation. Bookshelf One such mechanism is addition of more membrane via vesicle fusion (Fig 1B ). These same processes also work to dynamically control membrane fluidity by regulating the distribution of phospholipids, sphingolipids, and cholesterol in the membrane. PA is then used to create other phospholipids including PI, PC, PS, and PE, through the use of the DAG backbone. PMC The organization of lipids within the membrane also affects the structure of underlying cortical cytoskeleton. Each of these pathways that facilitate repair through membrane remodeling also alter the local composition and distribution of plasma membrane lipids in healthy cells (van Meer, 1989) (Figure 2D). Importantly, sequestration of cholesterol alone increased PLD activity, supporting the idea that transient increase in lipid fluidity after membrane injury may be required for PLD-mediated signaling. It has since become evident that in addition to resealing, remodeling of the plasma membrane through vesicle fusion (exocytosis), vesicle internalization (endocytosis), and shedding (ectocytosis) also contribute to the repair process (reviewed in (Horn & Jaiswal, 2018)). Liquids, mostly water, make up 70 to 90% of all living systems, and the loss of even a small percentage can mean the difference between life and death. Muscle fibers have a complex plasma membrane network with a repeating register of deep plasma membrane invaginations called the t-tubule network. Each of these lipids contributes their own qualities that affect the structural and signaling characteristics of the plasma membrane (Nicolson, 2014). Tam C, Idone V, Devlin C, Fernandes MC, Flannery A, He X, Andrews NW (2010). Very large plasma membrane disruptions (micron diameter) require membrane patching. Inclusion in an NLM database does not imply endorsement of, or agreement with, (D) The lipid make-up of the plasma membrane constantly changes. Intriguingly, PIP2 is needed for PLD activity suggesting the possibility that a feed-forward loop leads to increasing PIP2 concentrations as repair progresses ultimately facilitating the necessary build-up of F-actin (Figure 1B). Here the sugar (oligosaccharide) moiety faces the extracellular space interacting with other cells and extracellular ligands required for processes such as signaling, cell adhesion or intercellular interactions. Bethesda, MD 20894, Web Policies Tailored protection against plasmalemmal injury by annexins with different Ca2+ sensitivities, Sphingolipids and the formation of sterol-enriched ordered membrane domains, Plasma membrane repair is mediated by Ca2+-regulated exocytosis of lysosomes. This is notable because it is hypothesized that a beneficial role of decreasing membrane fluidity is preventing the spread of harmful lipid hydroperoxides, which likely form in the oxidative environment near the site of injury (Braughler & Hall, 1992; Hall, Wang, Miller, Cebak, & Hill, 2018). Interestingly, as a result of caveolae flattening, EHD2 dissociates from the plasma membrane and translocates to the nucleus where it alters gene transcription (Torrino et al., 2018). By clicking the Accept button you agree to the terms of our privacy policy. As discussed above, sphingolipids in the plasma membrane are an important regulator of plasma membrane repair. BMC Biol. 2015 Sep;45:2-9. doi: 10.1016/j.semcdb.2015.09.023. This dissociation has the effect of allowing Rho GTPase translocation to the membrane where it can interact with signaling lipids. Acute and chronic release of lipids and free fatty acids following cell and tissue injury has been widely recognized to be involved in the process of tuning the inflammatory and subsequent tissue repair response. Clipboard, Search History, and several other advanced features are temporarily unavailable. Corrotte M, Almeida PE, Tam C, Castro-Gomes T, Fernandes MC, Millis BA, Maugel TK. However, these repair activities can also be observed at the single-cell level. As described above, damage to the plasma membrane transiently increases the mobility of individual lipids. Exocytic fusion reduces membrane tension, and vesicle-vesicle fusion events provide a patch as a replacement for the membrane barrier missing at the disruption site. PI (3, 4, 5) P3 and PI (4, 5) P2 lipids target proteins with polybasic clusters to the plasma membrane, The membrane and lipids as integral participants in signal transduction: lipid signal transduction for the non-lipid biochemist. Inflammatory exudates provide insights into the regulation of the first stage of wound repair inflammation. Below we describe the biochemical signaling role of lipids in facilitating plasma membrane repair. A different model for plasma membrane repair began to emerge when mammalian cells injured mechanically or by SLO pores were found to undergo massive endocytosis, after Ca 2+ -triggered exocytosis of lysosomes ( Figure 1 C). Another role identified for lysosomal fusion in membrane repair is the secretion of the lipid modifying enzyme acid sphingomyelinase (ASM) (Defour et al., 2014; Tam et al., 2010). Instead, there exists distinct inter- and intra-leaflet heterogeneity of lipids. official website and that any information you provide is encrypted lipids) is one of the roles proposed for lysosome-mediated repair (Andrews et al., 2014; McNeil, 2002). While initial loss of cortical actin aids in repair by allowing physical access for vesicles to fuse with the plasma membrane, the accumulation of F-actin at the injury site in the minutes following injury, is also required to provide structural support to the repairing/repaired membrane and prevent additional injury due to membrane fragility (Demonbreun et al., 2016; Horn et al., 2017; Jaiswal et al., 2014; McDade, Archambeau, & Michele, 2014; Miyake et al., 2001). The reduction in membrane tension is likely due directly to the addition of phospholipids to reduced lipid packing, as well as due in part to the cytoskeletal remodeling associated with vesicular transport at the plasma membrane. Once membrane tension is restored, the poloxamer compound is forced out of the outer membrane leaflet (Houang, Sham, Bates, & Metzger, 2018). Lipids are a class of biomolecules, which are generally insoluble in water, and may refer to fatty acids, sterols, mono-, di-, and triglycerides, as well as phospholipids, among others. During the repair of sarcolemmal lesions, macrophages recognize exposed phosphatidylserine at the site of . Intriguingly, PA preferentially binds the Rho family member Rac1, resulting in nanocluster formation (Maxwell et al., 2018). To achieve these tasks, cells employ signaling networks, which respond to the changing microenvironment after injury and activate the diverse plasma membrane repair mechanisms with precise control in time and space. Plasma membrane repair in health and disease. Labazi M, McNeil AK, Kurtz T, Lee TC, Pegg RB, Angeli JPF, McNeil PL (2015). doi: 10.7554/eLife.80778. While membrane stabilization at the time of injury appears to improve membrane repair, a chronically rigid plasma membrane may inhibit the beneficial effects of transient lipid mobility after injury. When the cell is under stress, and the amount of ROS increases, the number of methionine "errors" is ramped up tenfold, allowing new proteins to be even more resistant to attack. Failure of injured cells to repair results in cell death and activates a tissue repair response. Analysis of Dysferlin Direct Interactions with Putative Repair Proteins Links Apoptotic Signaling to Ca. Among these lipids, PC is the most abundant in the plasma membrane and is formed by adding choline to the DAG backbone. Cholesterol and various proteins are also embedded within the . In the subsequent sections, we will discuss how this is achieved and utilized by the cell. The https:// ensures that you are connecting to the In response to an injury, a sudden change in hydrostatic pressure and local disassembly of the cortical cytoskeleton causes a rapid drop in membrane tension (Jaiswal et al., 2014; Miyake, McNeil, Suzuki, Tsunoda, & Sugai, 2001; Togo et al., 2000). Nam D. Jan 28, 2018 Because it has the Golgi apparatus Explanation: Actually it doesn't heal by itself it is helped by a cell organelle named Golgi apparatus. As structural components of the plasma membrane, lipids are responsible for contributing to membrane tension, rigidity, and overall shape. As MG53 interacts with the plasma membrane in a cholesterol-dependent manner ((Zhu et al., 2012); see Section 4), its extracellular role may involve a mode of action similar to poloxamer 188, where it inserts within membranes in a disordered lipid environment. However, in addition to this role, restoring membrane tension is another role that has been proposed for endocytosis after the membrane is resealed following a pore forming toxin injury (Skalman, Holst, Larsson, & Lundmark, 2018). Due to the differences in the three-dimensional conformations of membrane lipids, a change in their distribution changes the lipid packing density in a given lipid domain. Lipids act as signaling molecules through their ability to directly bind or otherwise alter the activity or localization of target proteins (Figure 2B, ,C).C). Similar to PS, DAG directly binds proteins to provide its signaling function; however, because it is generated de novo after injury, an additional temporal component to signaling is achieved. Godin LM, Vergen J, Prakash Y, Pagano RE, & Hubmayr RD (2011). Middel V, Zhou L, Takamiya M, Beil T, Shahid M, Roostalu U, Nienhaus GU (2016). In contrast, Annexin 1, one of the earliest responders to plasma membrane injury (Leikina et al., 2015; McNeil, Rescher, Gerke, & McNeil, 2006), does not appear to be essential for plasma membrane repair (Leikina et al., 2015; McNeil et al., 2006). Visualizing cytoplasmic flow during single-cell wound healing in Stentor coeruleus. These shortened sarcomeres induce a concomitant lengthening of adjacent sarcomeres and increased lateral strain to the plasma membrane. Given their ability to traverse away from the site of synthesis (Verweij et al., 2019), the EVs generated during plasma membrane injury may activate both local and distant tissue regeneration responses needed for repair. Modeling membrane shaping by proteins: Focus on EHD2 and NBAR domains. This results in the replacement of half of the body's adipocytes in 8 years. and transmitted securely. Minetti C, Sotgia F, Bruno C, Scartezzini P, Broda P, Bado M, Donati MA (1998). McNeil AK, Rescher U, Gerke V, & McNeil PL (2006). Proc Natl Acad Sci U S A. The membrane phosphoinositides, and PIP2 in particular, play an important role in regulating the interaction of F-actin with the plasma membrane (Kapus & Janmey, 2013; Saarikangas, Zhao, & Lappalainen, 2010). Weisleder N, Takizawa N, Lin P, Wang X, Cao C, Zhang Y, Chen P-J (2012). Dysferlin is not detected at injury sites until 10 s postinjury, a delay we attribute to an intermediary step involving calpain cleavage. Dysferlin-mediated phosphatidylserine sorting engages macrophages in sarcolemma repair. Eukaryotic cells have been confronted throughout their evolution with potentially lethal plasma membrane injuries, including those caused by osmotic stress, by infection from bacterial toxins and parasites, and by mechanical and ischemic stress. For example, membrane shedding is a known mechanism of plasma membrane repair, which functions to limit the lateral expansion of the wound area (Andrews, Almeida, & Corrotte, 2014; Horn & Jaiswal, 2018). Calcium can activate proteins directly, and ultimately is the initiator of many downstream repair pathways. Despite the many different types of tissue, there is a common repair program involved in tissue repair. The .gov means its official. 2022 May 15;23(10):5525. doi: 10.3390/ijms23105525. This structural arrangement is important for the organization of cholesterol in biological membranes as it results in the hydroxyl group associating with the neighboring lipid head groups and water, while the majority of the cholesterol molecule resides within the hydrophobic core of the membrane. In either case, the outward budding of the membrane produced by these ceramide-rich microdomains is thought to assist in microvesicle shedding. In fact, cells are able to perform hundreds, even thousands, of chemical transformations at the same time under life-friendly conditions (ambient temperature and pressure in an aqueous environment). During the S stage, the cell Activated calpains cleave dysferlin within a motif specifically encoded by alternately spliced exon 40a (230). Sood P, Lin A, Yan C, McGillivary R, Diaz U, Makushok T, Nadkarni AV, Tang SKY, Marshall WF. Cambridge (MA): Harvard Stem Cell Institute; 2008. While a common thread in lipid signaling is the modification of a target protein, either directly or indirectly, the numerous mechanisms lipids use to achieve this outcome allows for a great diversity of signaling. Cell Calcium. Being the most abundant component of the plasma membrane, lipids are also essential player in the process of plasma membrane repair; however, much of the research committed to identifying the mechanisms of plasma membrane repair has focused on the proteins associated with plasma membrane repair (Cooper & McNeil, 2015). Gurtner GC, Werner S, Barrandon Y, & Longaker MT (2008). Riazifar M, Pone EJ, Ltvall J, & Zhao W (2017). This is especially important for membrane signaling functions as the liquid-ordered domains often serve to aggregate membrane-associated proteins (Cebecauer et al., 2018). This study showed that endocytosis occurs after membrane resealing and is mediated by the CLIC/GEEC pathway effector GRAF1, which is implicated in repair of muscle fiber plasma membrane injury (Lenhart et al., 2015). Quantification of membrane tension after injury to fibroblasts demonstrated that a minimum tension force was reached by approximately 30 seconds post-injury, but tension was fully restored by 80 seconds post-injury (Togo et al., 2000). Water is essential to life. PIP2 dynamics after plasma membrane injury support a role for PIP2 in actin assembly during repair as its accumulation near the site of injury is generally delayed. Sreetama SC, Chandra G, Van der Meulen JH, Ahmad MM, Suzuki P, Bhuvanendran S, Jaiswal JK (2018). Translocation of existing lipid species to the site of injury provides a mechanism to recruit and activate protein machinery. Sci Rep. 2023 Mar 23;13(1):4763. doi: 10.1038/s41598-023-31973-2. An organelle (think of it as a cell's internal organ) is a membrane bound structure found within a cell. Such a role of CLIC/GEEC-mediated endocytosis in membrane remodeling is also supported by the observation that CLIC/GEEC is immediately activated in response to decreased membrane tension and has the capacity to turn over large amounts of plasma membrane (Thottacherry et al., 2018). Calcium also initiates lipid signaling after plasma membrane injury by activating phospholipases, such as phospholipase C (PLC). Cell wounding activates phospholipase D in primary mouse keratinocytes. Cell damage (also known as cell injury) is a variety of changes of stress that a cell suffers due to external as well as internal environmental changes. Marg A, Schoewel V, Timmel T, Schulze A, Shah C, Daumke O, & Spuler S (2012). An official website of the United States government. Microfluidic guillotine reveals multiple timescales and mechanical modes of wound response in Stentor coeruleus. We use cookies to give you the best browsing experience. Zhang KS, Blauch LR, Huang W, Marshall WF, Tang SKY. Alterations in Phosphatidylcholine Metabolism of StretchInjured Cultured Rat Astrocytes. Repair of injured plasma membrane by rapid Ca2+-dependent endocytosis, Lipid peroxidation induces cholesterol domain formation in model membranes. ESCRT machinery is required for plasma membrane repair. A decrease in membrane tension precedes successful cell-membrane repair. Honeybee immune systems depend more on protein diversity thanquantity. The site is secure. An official website of the United States government. Bomal E, Grandgeorge P, Yeo RJ, Candau N, Reis PM, Frauenrath H. Nat Commun. The lipids in the membrane control the function of the membrane - keeping some products inside and some outside. For example, a scallop prevents structural failure from fracture because its shell is comprised of two materials of varying stiffness. Biophys J. Other cells acquire specialized functions as they mature. This signaling function may occur due to the activity of the repair protein EHD2, which accumulates at the site of membrane injury and is thought to play a role in shaping membrane dynamics (Daumke et al., 2007; Demonbreun et al., 2016; Marg et al., 2012). cell, in biology, the basic membrane-bound unit that contains the fundamental molecules of life and of which all living things are composed. Repair of injured plasma membrane by rapid Ca2+-dependent endocytosis. (2011). sharing sensitive information, make sure youre on a federal Muscle fibers have a, Schematic representation of the structural, Schematic representation of the structural features of the protein families implicated in membrane, A cartoon depicting the potential role of dysferlin-mediated vesicle fusion in membrane repair., MeSH The role of lipids during plasma membrane repair goes far beyond a passive role in vesicle-mediated delivery of membrane lipids. One dead cell is not a big problem. Role of LBPA and Alix in multivesicular liposome formation and endosome organization, Rac1 nanoscale organization on the plasma membrane is driven by lipid binding specificity encoded in the membrane anchor. They include glycerophosphocholines, glycerophosphoglycerols, glycerophosphoinositols, as well as triacylglycerols (Taverna, Nanney, Pollins, Sindona, & Caprioli, 2011). While it is unclear whether caveolae can provide structural assistance to the damaged membrane in the context of a large membrane injury (as opposed to sub-injury threshold stress, (Sinha et al., 2011)), caveolae may still provide a signaling function during the repair process. Small GTPases, such as Rho family members, associate with biological membranes via lipid modifications (ten Klooster & Hordijk, 2007); however, selectivity for the plasma membrane is regulated through the polybasic domain comprised of a cluster of positively charged amino acids (Do Heo et al., 2006; Maxwell, Zhou, & Hancock, 2018). Role of calcium-sensor proteins in cell membrane repair. Zhu H, Lin P. h., De G, Choi K. h., Takeshima H, Weisleder N, & Ma J (2012). The plasma membrane itself forms the barrier responsible for the hydrostatic pressure experienced by the cell, while the cortical actin cytoskeleton, focal adhesions, and extracellular matrix regulate the structural tension (Burridge & Guilluy, 2016; Gauthier et al., 2012). (2017). Inositol is bound to the phosphate group in this phospholipid. Modular, cascade-like transcriptional program of regeneration in, R01 GM113602/GM/NIGMS NIH HHS/United States. 8600 Rockville Pike Johnson JL, Erickson JW, & Cerione RA (2012). PTRF presumably contributes to the translocation of MG53 to the injury-site, where MG53 is also able to bind PS and become activated in an oxidation-dependent manner (Cai et al., 2009). This phenomenon may be explained by the kinetic energy imparted on the membrane lipids by mechanical disruption, which can result in lipid mixing without relying on membrane tension (Petersen, Chung, Nayebosadri, & Hansen, 2016). In some cases, these forces are benign, such as membrane protrusion driven by cortical actin polymerization (Pontes, Monzo, & Gauthier, 2017). Moissoglu K, Kiessling V, Wan C, Hoffman BD, Norambuena A, Tamm LK, & Schwartz MA (2014). Cell membrane repair repurposes mechanisms from various cellular functions, including vesicle trafficking, exocytosis, and endocytosis, to mend the broken membrane. The cell membrane is an extremely pliable structure composed primarily of two layers of phospholipids (a "bilayer"). Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors. increased lipid fluidity described in Section 3) and allows for the membrane associated PLD to diffuse outward from lipid rafts and interact with PIP2 in order to metabolize PC. However, ceramide formation also changes membrane dynamics by forming rigid microdomains and potentially by displacing cholesterol from lipid rafts (London, 2004). Blauch LR, Gai Y, Khor JW, Sood P, Marshall WF, Tang SKY. Plasma membrane repair relies on the coordinated activity of repair machinery, which carries out vesicle fusion to the membrane, membrane shedding, and polymerization of F-actin at the site of repair (Horn & Jaiswal, 2018). Collectively, these changes enable lipids to initiate/regulate local signaling allowing precise spatial and temporal control over downstream plasma membrane repair pathways. Bissig C, Lenoir M, Velluz M-C, Kufareva I, Abagyan R, Overduin M, & Gruenberg J (2013). This is due to its protein-binding ability, resulting in protein translocation to the cholesterol-rich regions of plasma membrane (Sheng et al., 2012; Van Meer et al., 2008). This is in part achieved through the activity of lipid modifying enzymes, such as kinases, phosphatases, and phospholipases. Before In this review, we have discussed how lipids working at the individual as well as at the population level facilitate the proper orchestration of the repair response. There also exists lateral heterogeneity of lipid composition within each leaflet, which is demonstrated by the formation of lipid microdomains, such as the sphingomyelin and cholesterol-rich domains that exist interspersed among the phospholipids throughout the plasma membrane (Cebecauer et al., 2018; Sezgin, Levental, Mayor, & Eggeling, 2017) (Figure 2B). and transmitted securely. Lenhart KC, ONeill TJ, Cheng Z, Dee R, Demonbreun AR, Li J, Taylor JM (2015). Semin Cell Dev Biol. This cytoskeletal assembly is regulated by Rho GTPase activity, which triggers F-actin accumulation at the site of injury. How does the cell membrane self heal? They break down excess or worn-out cell parts. This may allow these lipids and proteins to interact with new partners that were unavailable due to spatial segregation prior to injury. This mechanism is particularly intriguing in light of the redox-sensitive nature of MG53. Elife. Federal government websites often end in .gov or .mil. This preferential association between different lipids results in an important feature of the plasma membrane its transverse and lateral heterogeneity. Formation of these outward budding vesicles at the plasma membrane is associated with an increase in cytosolic calcium and oxidation, as well as the disruption of the actin cytoskeletonplasma membrane interface (Pollet, Conrard, Cloos, & Tyteca, 2018), and each of these occurs locally in the immediate aftermath of membrane injury (Andrews et al., 2014; Horn & Jaiswal, 2018). The discussion above illustrates several roles for lipids in changing biophysical properties of the injured plasma membrane during repair. This raises the intriguing possibility that MG53 may affect plasma membrane structural properties. MG53 (40) shows diffuse enrichment at injury sites within 2 s of membrane injury in a calcium-independent manner (150). government site. EVs are known to be generated in response to plasma membrane injury of single cells, and this is required for successful repair (Jimenez et al., 2014; Scheffer et al., 2014). J Cell Biol. SM utilizes the ceramide (Cer) backbone and can be used to generate the signaling lipid sphingosine-1-phosphate (S1P). Disclaimer. 2022 Aug 23;13(1):4950. doi: 10.1038/s41467-022-31277-5. Calise S, Blescia S, Cencetti F, Bernacchioni C, Donati C, & Bruni P (2012). Single-molecule tracking of small GTPase Rac1 uncovers spatial regulation of membrane translocation and mechanism for polarized signaling, Proceedings of the National Academy of Sciences. These remodeling events actively promote plasma membrane repair; however, they also act as extensions of the repair response and may continue long after successful resealing in order to restore the plasma membrane to its pre-injury state. Bianco F, Perrotta C, Novellino L, Francolini M, Riganti L, Menna E, Clementi E. (2009). Lamb RG, Harper CC, McKinney JS, Rzigalinski BA, & Ellis EF (1997). Copyright 2017, American Association for the Advancement of Science. 2008 Mar 10;180(5):905-14. doi: 10.1083/jcb.200708010. Epub 2008 Mar 3. Different cell-intrinsic PM repair mechanisms have been reported, including membrane fusion and replacement strategies (via exocytosis-mediated repair), removal of damaged membranes (by. Cell Regen. Palmitate-mediated disruption of the endoplasmic reticulum decreases intracellular vesicle motility. There are mechanisms that allow some products to enter or leave the cell either actively or passively. Vaughan EM, You J-S, Yu H-YE, Lasek A, Vitale N, Hornberger TA, & Bement WM (2014). Bi G-Q, Alderton JM, & Steinhardt RA (1995). Abstract. Tools. Damage control: cellular mechanisms of plasma membrane repair. Living systems do this using structures or waterproof materials to prevent or slow liquid movement. To do so, they must control the movement of liquids across their boundaries. Presence of PS at the free membrane wound edge helps directs the annexin proteins to this site in a calcium-dependent manner, where they perform vital functions required for stabilization and shaping of the repairing membrane (see Section 3.3). Togo T, Krasieva TB, & Steinhardt RA (2000). The most abundant component of the cells plasma membrane is the lipids. This allows local and functional diversity between the two leaflets as well as various parts of the single contiguous plasma membrane (Figure 2B). 2022 Dec 14;10(12):3256. doi: 10.3390/biomedicines10123256. Multiplexed molecular descriptors of pressure ulcers defined by imaging mass spectrometry, Targeting and localized signalling by small GTPases. When cells have DNA damage but fail to undergo apoptosis, they may be on the road to cancer. Stem cells in animal models of regeneration. Sphingomyelin also confers different properties to the plasma membrane than the phospholipids, not least due to its preferential association with sterols (Ramstedt & Slotte, 2006). diacylglycerol - DAG) backbone are called glycerophospholipids (referred to as phospholipids hereafter) and make up the majority of the plasma membrane. Without adequate remodeling, the plasma membrane protein and lipid composition would change dramatically, particularly after repeat injuries, and no longer function as in its pre-injury state. These enzymes initiate signaling through the generation of new lipid species, providing an added spatial, as well as a temporal component to lipid signaling, helping to more precisely coordinate the repair response. Further, PA is implicated in processes critical to the success of membrane repair such as vesicle fusion with the plasma membrane and GTPase signaling (Cazzolli et al., 2006; Zhang & Du, 2009). Similar to PLC, phospholipase D (PLD) activity is also increased after injury and is required for repair (Arun et al., 2013). Epub 2008 Oct 9. Lipids contribute to cellular physiology at both an individual and population level. Eukaryotic cells have been shown to utilize calcium-activated exocytosis to reduce membrane tension and promote repair via lipid-disorder driven attractions.
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