For example, when humans receive a cut, they must limit blood loss. The radiation could prevent the DNA from replicating correctly. PMC Poloxamer 188 facilitates the repair of alveolus resident cells in ventilator-injured lungs, American journal of respiratory and critical care medicine. . Regulation of the actin cytoskeleton-plasma membrane interplay by phosphoinositides. Houang EM, Haman KJ, Filareto A, Perlingeiro RC, Bates FS, Lowe DA, & Metzger JM (2015). Collectively, these changes enable lipids to initiate/regulate local signaling allowing precise spatial and temporal control over downstream plasma membrane repair pathways. The MG53 binding protein PTRF (cavin-1) binds cholesterol in response to membrane injury (Zhu et al., 2012). Furthermore, exposure of the plasma membrane hydrophobic core as a result of reduced lipid packing provides the opportunity for injury-triggered lipid signaling through the binding of cholesterol (see Section 4). Abrams ST, Wang L, Yong J, Yu Q, Du M, Alhamdi Y, Cheng Z, Dart C, Lane S, Yu W, Toh CH, Wang G. Biomedicines. The wounded cell can survive if a rapid repair respons Membrane Repair: Mechanisms and Pathophysiology These observations suggest that lipids are not bystanders during the repair process, but are instead actively involved in organizing the playing field on which repair machinery operates. Gurtner GC, Werner S, Barrandon Y, & Longaker MT (2008). These same processes also work to dynamically control membrane fluidity by regulating the distribution of phospholipids, sphingolipids, and cholesterol in the membrane. Cong X, Hubmayr RD, Li C, & Zhao X (2017). Requirement for annexin A1 in plasma membrane repair, Repairing a torn cell surface: make way, lysosomes to the rescue, Plasma membrane disruption: repair, prevention, adaptation, Annual review of cell and developmental biology, Coping with the inevitable: how cells repair a torn surface membrane, Biochemistry of lipids, lipoproteins and membranes. The .gov means its official. Charged phospholipids such as PIP2, PS, and PE are almost exclusively found on the inner leaflet, while the glycosphingolipids are only found on the outer leaflet. During the G1 stage, the cell prepares for division by increasing its mass. Gazzerro E, Sotgia F, Bruno C, Lisanti MP, & Minetti C (2010). Bomal E, Grandgeorge P, Yeo RJ, Candau N, Reis PM, Frauenrath H. Nat Commun. However, ceramide formation also changes membrane dynamics by forming rigid microdomains and potentially by displacing cholesterol from lipid rafts (London, 2004). Because membrane tension limits the ability of cellular membranes to self-seal, cellular mechanisms that reduce membrane tension can promote membrane sealing. Zuzek A, Fan JD, Spaeth CS, & Bittner GD (2013). This preferential association between different lipids results in an important feature of the plasma membrane its transverse and lateral heterogeneity. If you break a bone, your body immediately begins producing new cells to heal the damage. 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. Kinetic disruption of lipid rafts is a mechanosensor for phospholipase D, Conversion of phosphatidylcholine to phosphatidylglycerol with phospholipase D and glycerol, Journal of the American Oil Chemists Society. EHD2 localization at caveolae results from its affinity for phosphatidylinositol 4,5-bisphosphate (PIP2), which is enriched around the caveolae boundary (Parton & Del Pozo, 2013; Simone, Caplan, & Naslavsky, 2013). 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). For example, Annexin 5 accumulates first to form a lattice structure, which provides a force opposing the tension at the wound edge (Bouter et al., 2011). Please enable it to take advantage of the complete set of features! Gauthier NC, Masters TA, & Sheetz MP (2012). Lethal Injury (Cell Death) In many situations, the damage to a cell may be so severe that the cell cannot survive. Marmots maintain strong bones during hibernation by building up without breakingdown. 2022 Dec 14;10(12):3256. doi: 10.3390/biomedicines10123256. Unauthorized use of these marks is strictly prohibited. Diz-Muoz A, Fletcher DA, & Weiner OD (2013). Further, PE and PC head groups can be cleaved and replaced with serine to produce PS (Oropeza, 2017). Membrane repair is a conserved physiologic process in multiple tissues Organ Type of mechanical force Principal cells stressed Cell wounding 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. Use of lipidomics during epidermal wound repair identified that several of the plasma membrane lipids discussed above are enriched during wound repair. Epub 2023 Mar 3. Das S, Yin T, Yang Q, Zhang J, Wu YI, & Yu J (2015). Similar to the changes in tension described above, the fluidity of the plasma membrane is also dynamic after injury. It can also be produced by methylation of existing PE, while PE can be produced by the decarboxylation of PS. As a library, NLM provides access to scientific literature. These observations on PIP2 kinetics line up remarkably well with the accumulation of F-actin at the injury site, which begins around 30 seconds after injury and extends for several minutes (Godin, Vergen, Prakash, Pagano, & Hubmayr, 2011; Horn et al., 2017). Limiting the spread of lipid hydroperoxides may also explain the beneficial effect of vitamin E treatment on plasma membrane repair (Howard, McNeil, & McNeil, 2011; Labazi et al., 2015). lipids) is one of the roles proposed for lysosome-mediated repair (Andrews et al., 2014; McNeil, 2002). From PA, cells generate DAG, or cytidine diphosphate-DAG (CDP-DAG), which serve as inputs into the phospholipid biosynthetic pathways (Figure 1A, ,B).B). Compared with cytosolic antioxidants, which can be detrimental to repair (Spaeth et al., 2012), vitamin E is membrane-localized and could therefore allow for the local buildup of oxidized lipids at the site of injury while preventing the global spread of lipid oxidation. Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors. The plasma membrane is not a homogenous mixture of the different lipids described above (Figure 2A). Definition. calcium, which when constantly increased, induces apoptosis. 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). However, shear force on the membrane increases the kinetic energy required for lipid mixing (i.e. Epub 2008 Mar 3. The observation, that endocytosis may not be required for resealing through the removal of pore-forming toxins but instead acts as a mechanosensor to buffer membrane tension, may also explain how endocytosis participates in the repair of mechanical damage, where no membrane-spanning pores need to be removed. However, whether caveolae facilitate repair by buffering membrane tension remains unclear because, unlike the capacity of CLIC/GEEC endocytosis, caveolae make up a small portion (as small as 0.03%) of the membrane area and are not found ubiquitously in all cells (Gauthier et al., 2012; Sinha et al., 2011). 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. Cheng JP, Mendoza-Topaz C, Howard G, Chadwick J, Shvets E, Cowburn AS, Nichols BJ (2015). Cells (whether entire unicellular organisms or parts of multicellular living systems) grow, metabolize nutrients (that is, chemically transform them), produce proteins and enzymes, replicate, and move. Annexin A4 and A6 induce membrane curvature and constriction during cell membrane repair, Involvement of lipid peroxidation in CNS injury, Focal adhesions, stress fibers and mechanical tension. 2008 Nov;18(11):552-9. doi: 10.1016/j.tcb.2008.09.001. Plasma membrane damage needs to be rapidly repaired to avoid cell death. Along with the annexins, which act quickly to physically manipulate the membrane itself, reassembly of the cytoskeleton plays a crucial role in restoring membrane tension in the later stages of repair. While PLD is also activated by calcium, recent findings have provided insight into the role of mechanical stress on initiating lipid signaling regulated by PLD (Petersen et al., 2016). This causes the exposure of the membrane hydrophobic core and allows proteins to interact with cholesterol. Negative membrane curvature catalyzes nucleation of endosomal sorting complex required for transport (ESCRT)-III assembly. The lipid-mediated cytoskeletal rearrangement described above provides the cell with a mechanism to close the wounded site and add structural support to the newly resealed membrane. Dysferlin regulates cell membrane repair by facilitating injury-triggered acid sphingomyelinase secretion, Demonbreun AR, & McNally EM (2016). Cell membrane repair repurposes mechanisms from various cellular functions, including vesicle trafficking, exocytosis, and endocytosis, to mend the broken membrane. Front Cell Dev Biol. the contents by NLM or the National Institutes of Health. 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)). Along with DAG, IP3 is also generated by the activity of PLC. To regulate the composition of plasma membrane lipids, cells utilize vesicle trafficking, which can add lipids (by exocytosis) or remove lipids (by endocytosis) from the plasma membrane. Unlike Annexin 5 that forms a lattice structure at the wound edge (Bouter et al., 2011), Annexins A4 and A6 work together to mediate constriction of the wounded edges of the plasma membrane, aiding in the closure of the wound (Boye et al., 2017). The physical and molecular mechanisms by which a cell can heal membrane ruptures and rebuild damaged or missing cellular structures remain poorly understood. Transient change in lipid mobility can have many effects on plasma membrane function related to both structure and signaling, and deciphering which of these are beneficial for repair requires further studies. Mammals make up less than 1% of all animals on earth, but they include some of the most well-known species. This Goldilocks principle applies to several aspects of lipid involvement in the repair process. When cells have DNA damage but fail to undergo apoptosis, they may be on the road to cancer. This can limit the expansion of the wound area itself. Arp2/3-mediated F-actin formation controls regulated exocytosis in vivo. Not only is the composition and organization of the plasma membrane in constant flux, the membrane itself also must interact with forces being applied to it from all directions. For example, caveolae are the site for assembling membrane repair proteins such as EHD2 and MG53 (Cai et al., 2009; Daumke et al., 2007; Marg et al., 2012). The plasma membrane has a unique lipid composition that helps distinguish its structural and functional properties from the other internal membrane-bound compartments. Sci Rep. 2023 Mar 23;13(1):4763. doi: 10.1038/s41598-023-31973-2. HHS Vulnerability Disclosure, Help Stem cell extracellular vesicles: extended messages of regeneration, Annual review of pharmacology and toxicology. This is achieved in part through the activity of lipid modifying enzymes, such as phospholipases, which are activated by the changing biochemical environment after injury. Spatiotemporal dynamics of actin remodeling and endomembrane trafficking in alveolar epithelial type I cell wound healing. The radiation could pass through the cell without damaging the DNA. Modeling membrane shaping by proteins: Focus on EHD2 and NBAR domains. This site needs JavaScript to work properly. Do Heo W, Inoue T, Park WS, Kim ML, Park BO, Wandless TJ, & Meyer T (2006). PMC 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. Membrane damage: Damage to the cell membrane disturbs the state of cell electrolytes, e.g. In mammalian cells the majority of cellular cholesterol is found in the plasma membrane, where it can make up to 50% of lipid content (Van Meer, Voelker, & Feigenson, 2008). Neurite transection produces cytosolic oxidation, which enhances plasmalemmal repair. This study showed that shear force on the membrane, as experienced by cells during mechanical injury, facilitated increased PLD activity through the process of lipid mixing. This process is itself facilitated by mechanisms that regulate membrane tension, in particular the re-establishment of the actin cortex. Pollet H, Conrard L, Cloos A-S, & Tyteca D (2018). Cebecauer M, Amaro M, Jurkiewicz P, Sarmento M. J. o., achl R, Cwiklik L, & Hof M (2018). Spontaneous formation of a self-healing carbon nanoskin at the liquid-liquid interface. Muscle membrane integrity in Duchenne muscular dystrophy: recent advances in copolymer-based muscle membrane stabilizers. For example, a scallop prevents structural failure from fracture because its shell is comprised of two materials of varying stiffness. Architectural and mechanistic insights into an EHD ATPase involved in membrane remodelling. Once membrane tension is restored, the poloxamer compound is forced out of the outer membrane leaflet (Houang, Sham, Bates, & Metzger, 2018). During regeneration, sphingolipids such as sphingosine 1-phosphate (S1P) are known for their growth promoting effect on tissue resident stem cells (Calise et al., 2012; Nojima, Freeman, Gulbins, & Lentsch, 2015). Scattered throughout the bloodstream are lens-shaped structures that serve to plug thewound. The fluidity of the membrane is determined in part by its composition, with cholesterol and sphingolipid-rich regions being less fluid than those areas comprised primarily of phospholipids. FOIA 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. 'Resealing' is the emergency response required for cell . Sphingolipids in liver injury, repair and regeneration, Development of Biomimetic Membrane Assemblies on Microspheres for High-Throughput and Multiplexable Studies, Caveolae as plasma membrane sensors, protectors and organizers. Cell damage can be reversible or irreversible. Boye TL, Maeda K, Pezeshkian W, Snder SL, Haeger SC, Gerke V, Nylandsted J. Phospholipids can switch the GTPase substrate preference of a GTPase-activating protein, Ceramide selectively displaces cholesterol from ordered lipid domains (rafts) implications for lipid raft structure and function. Inclusion in an NLM database does not imply endorsement of, or agreement with, Lysosomes are involved with various cell processes. Horn A, Van der Meulen JH, Defour A, Hogarth M, Sreetama SC, Reed A, Jaiswal JK. This is called apoptosis. Mechanochemical feedback control of dynamin independent endocytosis modulates membrane tension in adherent cells, Long-term Potentiation of Wound-induced Exocytosis and Plasma Membrane Repair Is Dependant on cAMP-response Element-mediated Transcription via a Protein Kinase C-and p38 MAPK-dependent Pathway. Additional structural changes the plasma membrane must adopt for repair include molding the shape of the membrane to limit wound expansion as well as pulling in the membrane edges to close the wound. Each month, well bring you a selection of compelling updates to this ever-growing library of biological strategies and innovations. A lysosome is a membrane-bound cell organelle that contains digestive enzymes. This process is more efficient when GTPases and their regulatory proteins (which are themselves regulated by lipids) are clustered (Ligeti, Dagher, Hernandez, Koleske, & Settleman, 2004). 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). While intracellular MG53 is a redox-sensitive protein capable of facilitating vesicle aggregation, it is proposed to have multiple functions during membrane repair. Thus, each of these lipids contributes significantly to the organization, structure, and function of the plasma membrane as a whole. This may allow these lipids and proteins to interact with new partners that were unavailable due to spatial segregation prior to injury. 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. Plasma membrane repair in health and disease. While being a mostly non-polar molecule, owing to its steroid backbone and hydrocarbon chain, cholesterol does possess a hydroxyl group opposite the hydrocarbon chain. Slabodnick M, Prevo B, Gross P, Sheung J, Marshall W. J Vis Exp. PA is itself generated primarily from glycerol-3-phosphate, which is a product of glycolysis. Accumulation of PS at the site of membrane injury allows it to act as a damage sensor, marking a key site for the recruitment of repair proteins such as annexins (Boye et al., 2017). In this way, lipids play an important role in polarizing the cellular response to an injury. Unauthorized use of these marks is strictly prohibited. All RightsReserved. This process, facilitated by the dysferlin-mediated release of acid sphingomyelinase (Defour et al., 2014) creates microdomains of ceramide from sphingomyelin. This method of extracellular communication may allow for the proper execution of inflammatory and regenerative responses needed for appropriate tissue remodeling required to restore organ function. Sarcolemmal repair is a slow process and includes EHD2, Effect of oxidative stress on membrane structure: small-angle X-ray diffraction analysis. We have briefly discussed how such an integral role of lipids in plasma membrane repair also extends into tissue-level repair and restoration of organ function. and transmitted securely. However, excessive force applied to the membrane can result in physical damage, such as the shear force applied on the endothelial cells by blood flow, on muscle cells during contraction, on lung alveolar cells during breathing, or by a blunt force trauma to any cell (Cong, Hubmayr, Li, & Zhao, 2017; Demonbreun & McNally, 2016; McNeil & Steinhardt, 2003). Annexins are a class of calcium-sensitive proteins that rapidly accumulate at the site of a membrane injury (Potez et al., 2011). PI5K activity is itself driven by regulators of membrane repair including Rho GTPases (Gilmore & Burridge, 1996) and PLD (Roach et al., 2012). This allows for the movement and patterning of lipids into signaling domains, changing the spatial arrangement of proteins that selectively interact with a particular lipid species. Thus, while increase in lipid mobility following plasma membrane injury is associated with successful repair, excessive lipid mobility leading to membrane instability is detrimental to the repair process. Zhu H, Lin P. h., De G, Choi K. h., Takeshima H, Weisleder N, & Ma J (2012). Plasma membrane lipids can be grouped into three classes glycerophospholipids, sphingolipids, and sterols. Rather than these roles being separated from each other, they overlap significantly such that one can easily be an extension of the other. Two-way traffic on the road to plasma membrane repair. While this mechanism outlines how ESCRT proteins assemble, the lipid signaling that determines the appropriate spatial localization relative to the membrane injury in order to limit wound expansion has not been elucidated. Each of these provides another mechanism for generating specific membrane lipids acutely in parallel to biosynthetic inputs. Cai C, Masumiya H, Weisleder N, Matsuda N, Nishi M, Hwang M, Zhao X. Dystrophic heart failure blocked by membrane sealant poloxamer, Cytosolic proteins can exploit membrane localization to trigger functional assembly, Phospholipids in animal eukaryotic membranes: transverse asymmetry and movement, Phosphatidic acid signaling regulation of Ras superfamily of small guanosine triphosphatases, Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids. Plasma membrane lipids help with successful repair by being part of the affected entity that also works to sense membrane injury, providing spatial and temporal cues to trigger signaling for downstream repair pathways, and ultimately being the benefactor of the successful wound repair response. (D) The lipid make-up of the plasma membrane constantly changes. Cholesterol interacts with both phospholipids and sphingolipids, and its interactions with these lipids play a crucial role in determining the overall physical properties of the plasma membrane. official website and that any information you provide is encrypted Damage control: cellular mechanisms of plasma membrane repair. One model explaining membrane injury in dystrophin-deficient muscle fibers proposes that an initial injury causes a local influx of calcium and a local region of hypercontraction.
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