how does a cell membrane repair itself

Cell membrane | Definition, Function, & Structure | Britannica The physical and molecular mechanisms by which a cell can heal membrane ruptures and rebuild damaged or missing cellular structures remain poorly understood. 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). Lethal Injury (Cell Death) In many situations, the damage to a cell may be so severe that the cell cannot survive. BMC Biol. J Cell Biol. However, these repair activities can also be observed at the single-cell level. 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. In general, PIP2 is a positive regulator of F-actin polymerization and the presence of PIP2 increases the stability of the actin cytoskeletonplasma membrane interface. Dysferlin-mediated phosphatidylserine sorting engages macrophages in sarcolemma repair. Just like cells have membranes to hold everything in, these mini-organs are also bound in a double layer of phospholipids to insulate their little compartments within the larger cells. For plasma membrane repair to occur successfully, the cell must possess a means to sense that injury has occurred, coordinate the change in activity and localization of repair machinery, and ultimately close the wounded area. HHS Vulnerability Disclosure, Help PC), with a conical shaped, charged phospholipid (e.g. One such mechanism is addition of more membrane via vesicle fusion (Fig 1B ). These lipids also exist at the boundary of lipid-ordered domains, such as lipid rafts, indicating that GTPases are targeted to these regions where protein accumulation at the membrane is common (Moissoglu et al., 2014), increasing their relative signaling capacity. The signaling lipid PS is interesting in this regard due to its localization to the wound edge after injury. Cholesterol and various proteins are also embedded within the . 2023 Feb 28;24(5):4707. doi: 10.3390/ijms24054707. In this review, we will focus on the role of lipids during plasma membrane repair by discussing their functions as both structural and signaling molecules. Unauthorized use of these marks is strictly prohibited. Van Meer G, Voelker DR, & Feigenson GW (2008). During the S stage, the cell The organization of lipids within the membrane also affects the structure of underlying cortical cytoskeleton. Blood cells called platelets release clotting factors to stop the bleeding; white blood cells rid the area of foreign materials and release molecules to coordinate healing; cells called fibroblasts start rebuilding using proteins called collagen; new blood vessels form; and skin cells called keratinocytes create the newsurface. Sphingosine 1-phosphate stimulates proliferation and migration of satellite cells: role of S1P receptors, Biochimica et Biophysica Acta (BBA)-Molecular Cell Research. Trends Cell Biol. Bookshelf Cell before mitosis showing the location of the centrioles, microtubules, nuclear membrane, nucleolus, and DNA (Let's Talk Science using an image by Aldona via iStockphoto). The structural role of lipids described above illustrates how their ability to modify the biophysical properties of the plasma membrane is beneficial for resealing. 2018 Apr 23;28(8):R392-R397. Myofiber injury in zebrafish was found to cause rapid loss of PIP2, followed by restoration to pre-injury levels by 30 seconds post-injury (Middel et al., 2016). Modeling membrane shaping by proteins: Focus on EHD2 and NBAR domains. ESCRT assembly for membrane shedding is activated by the calcium-dependent ALG-2 protein, which then recruits its interacting partner ALIX leading to subsequent recruitment of the remaining complex members (Scheffer et al., 2014). If you break a bone, your body immediately begins producing new cells to heal the damage. Below we describe the biochemical signaling role of lipids in facilitating plasma membrane repair. 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). Annexins are a class of calcium-sensitive proteins that rapidly accumulate at the site of a membrane injury (Potez et al., 2011). Clipboard, Search History, and several other advanced features are temporarily unavailable. sharing sensitive information, make sure youre on a federal The lipids in the membrane control the function of the membrane - keeping some products inside and some outside. Heier CR, Damsker JM, Yu Q, Dillingham BC, Huynh T, Van der Meulen JH, Scheffer L. (2013). Spatial arrangement of lipids is also known to regulate Rho family GTPase activity (see Section 4.3). These same processes also work to dynamically control membrane fluidity by regulating the distribution of phospholipids, sphingolipids, and cholesterol in the membrane. Johnson JL, Erickson JW, & Cerione RA (2012). Cholesterol modulates cell signaling and protein networking by specifically interacting with PDZ domain-containing scaffold proteins. Calcium-activated exocytosis reduces membrane tension and promotes spontaneous repair driven by lipid disorder for injuries hundreds of nanometers in diameter. Repeated eccentric exercise in healthy subjects (i.e., stepping down for 20 min) is known to induce damage so severe that muscle fibers degenerate over the following days and weeks (91, 131, 199). 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). Spaeth C, Fan J, Spaeth E, Robison T, Wilcott R, & Bittner G (2012). "Knowledge of how single cells repair and regenerate themselves underpins our mechanistic understanding of cell biology and could guide treatments for conditions involving cellular damage." These examples illustrate the ability of cells to heal wounds and regenerate missing structures. Phospholipids in particular show inter-leaflet heterogeneity. 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). We will highlight how lipids respond to injury and facilitate repair both at the level of individual molecules and at the bulk level by collectively altering the plasma membrane form and function. When . The antioxidant requirement for plasma membrane repair in skeletal muscle. The plasma membrane has a unique lipid composition that helps distinguish its structural and functional properties from the other internal membrane-bound compartments. It can also be produced by methylation of existing PE, while PE can be produced by the decarboxylation of PS. The tight packing, along with the preference of cholesterol to intercalate the acyl chains of sphingomyelin creates the liquid-ordered membrane domains, such as the so-called lipid rafts (Van Meer et al., 2008) (Figure 2C). In order to balance any decrease in membrane tension, such as that caused by exocytosis, cells routinely utilize endocytosis, which reduces the membrane area and results in increased tension (Dai & Sheetz, 1995). Rather than these roles being separated from each other, they overlap significantly such that one can easily be an extension of the other. There are mechanisms that allow some products to enter or leave the cell either actively or passively. Thus, it is clear that there is a need to acknowledge the role of lipids as an active participant in the processes of both cell and tissue repair. Interphase has three stages: G1, S and G2. Cells are the basic building blocks of all living systems, so cellular processes dictate how physiological processes occur within those systems. Arp2/3-mediated F-actin formation controls regulated exocytosis in vivo. Drescher DG, Drescher MJ, Selvakumar D, Annam NP. C-terminal di-arginine motif of Cdc42 protein is essential for binding to phosphatidylinositol 4, 5-bisphosphate-containing membranes and inducing cellular transformation, Plasma membraneCortical cytoskeleton interactions: A cell biology approach with biophysical considerations, Control of diverse subcellular processes by a single multi-functional lipid phosphatidylinositol 4, 5-bisphosphate [PI (4, 5) P2], The structural role of cholesterol in cell membranes: from condensed bilayers to lipid rafts.

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