The endomembrane requirement for cell surface repair

McNeil, Paul L.; Miyake, Katsuya; Vogel, Steven S.

doi:10.1073/pnas.0736739100

Cited by 136 publications

(109 citation statements)

References 34 publications

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“…Although long-lived (e.g., >100 s) increases of TMC were observed (e.g., The existence of two distinctive recovery constants may reflect the different time scale of the mechanisms involved in cell membrane repair (31,32), including extracellular Ca 2þ -triggered homotypic membrane-fusion events that occur on a subsecond time scale, and facilitated self-sealing that is caused by reduction of membrane tension by exocytosis and believed to be associated with small membrane disruptions. The slow time constant may represent the relatively slow homotypic membrane fusion whereas the fast recovery constant may be associated with facilitated sealing, which is determined by the physical property of the specific membrane of each cell type.…”

Section: Resultsmentioning

confidence: 99%

Spatiotemporally controlled single cell sonoporation

Fan

Liu

Mayer

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

209

215

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This paper presents unique approaches to enable control and quantification of ultrasound-mediated cell membrane disruption, or sonoporation, at the single-cell level. Ultrasound excitation of microbubbles that were targeted to the plasma membrane of HEK-293 cells generated spatially and temporally controlled membrane disruption with high repeatability. Using whole-cell patch clamp recording combined with fluorescence microscopy, we obtained time-resolved measurements of single-cell sonoporation and quantified the size and resealing rate of pores. We measured the intracellular diffusion coefficient of cytoplasmic RNA/DNA from sonoporation-induced transport of an intercalating fluorescent dye into and within single cells. We achieved spatiotemporally controlled delivery with subcellular precision and calcium signaling in targeted cells by selective excitation of microbubbles. Finally, we utilized sonoporation to deliver calcein, a membrane-impermeant substrate of multidrug resistance protein-1 (MRP1), into HEK-MRP1 cells, which overexpress MRP1, and monitored the calcein efflux by MRP1. This approach made it possible to measure the efflux rate in individual cells and to compare it directly to the efflux rate in parental control cells that do not express MRP1.D espite the development of various approaches for transporting membrane-impermeant compounds (such as fluorescent markers, DNA, RNA, siRNA, proteins, peptides, and amino acids) into living cells (1-3), efficient intracellular delivery of bioactive agents for biomedical applications with minimal adverse effects remains challenging. In addition, it is desirable yet difficult to achieve local perturbation of intracellular processes, which requires subcellular molecular localization inside the living cell (4, 5).Sonoporation uses ultrasound to induce transient disruption of cell membranes (6-8), thereby enabling transport of membraneimpermeant compounds into the cytoplasm of living cells (6,(9)(10)(11). Without the need to use viral vectors, sonoporation enables the delivery of a wide range of bioactive agents with minimal inflammatory and immunological responses for both in vitro studies and in vivo applications (12-16). In addition, ultrasound application can be targeted to a specific volume of tissue in vivo noninvasively. These unique characteristics make sonoporation a compelling and versatile technology for nonviral drug and gene delivery.Sonoporation is typically performed for bulk treatment of a tissue volume in vivo or a large number of cells in vitro, often facilitated by microbubbles that are either injected in the vasculature or mixed in solution with suspended or attached cells. Ultrasound application induces cavitation of the microbubbles (17), signified by rapid volume expansion/contraction and/or collapse (18). These effects generate localized fluid flow, shear stress, and other mechanical or physical impact capable of affecting cells and structures nearby (7,19,20).However, the detailed processes supporting sonoporationmediated transmembrane and ...

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Section: Resultsmentioning

confidence: 99%

Spatiotemporally controlled single cell sonoporation

Fan

Liu

Mayer

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

209

215

View full text Add to dashboard Cite

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“…This is best demonstrated in red blood cells (40). However, most plasma membrane lesions, particularly if they are large, repair only if intracellular lipids are shuttled to the plasma membrane by an active, energy-dependent, and Ca 2ϩ -regulated process (41)(42)(43). The insertion of lipids into the plasma membrane causes a fall in plasma membrane tension, which in turn promotes "self-sealing" by lateral lipid flow (44,45).…”

Section: Molecular Mechanisms Of Plasma Membrane Repairmentioning

confidence: 99%

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

Doerr

Gajić

Berríos

et al. 2005

Am J Respir Crit Care Med

118

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The objective of this study was to assess the effects of hypercapnic acidosis on lung cell injury and repair by confocal microscopy in a model of ventilator-induced lung injury. Three groups of normocapnic, hypocapnic, and hypercapnic rat lungs were perfused ex vivo, either during or after injurious ventilation, with a solution containing the membrane-impermeant label propidium iodide. In lungs labeled during injurious ventilation, propidium iodide fluorescence identifies all cells with plasma membrane wounds, both permanent and transient, whereas in lungs labeled after injurious ventilation propidium iodide fluorescence identifies only cells with permanent plasma membrane wounds. Hypercapnia minimized the adverse effects of high-volume ventilation on vascular barrier function, whereas hypocapnia had the opposite effect. Despite CO 2 -dependent differences in lung mechanics and edema the number of injured subpleural cells per alveolus was similar in the three groups (0.48 Ϯ 0.34 versus 0.51 Ϯ 0.19 versus 0.43 Ϯ 0.20 for hypocapnia, normocapnia, and hypercapnia, respectively). However, compared with normocapnia the probability of wound repair was significantly reduced in hypercapnic lungs (63 versus 38%; p Ͻ 0.02). This finding was subsequently confirmed in alveolar epithelial cell scratch models. The potential relevance of these observations for lung inflammation and remodeling after mechanical injury is discussed.Keywords: permissive hypercapnia; plasma membrane wounding and repair; ventilator-induced lung injury So-called lung protective mechanical ventilation strategies emphasize lung recruitment and the avoidance of large tidal volumes. Such strategies are often associated with hypercapnic acidosis. Many experts view "permissive hypercapnia" as a necessary evil of a low tidal ventilation strategy (1). Concern about detrimental effects of acidemia on renal and cardiovascular function have motivated attempts to enhance CO 2 removal by tracheal gas insufflation (2) and have led to unsubstantiated recommendations about the use of bicarbonate buffers in hypercapnic patients (3). More recent data suggest that hypercapnia may actually protect the lung from certain manifestations of ischemiareperfusion, endotoxin, and mechanical ventilation-related injury (4-9). Hypocapnia, in contrast, and correction of acidemia may be harmful (10-12). The specific mechanisms through which hypercapnia influences lung injury and vascular barrier function remain uncertain (13). CO 2 generates H ϩ ions, which react with titratable groups in certain amino acids and/or interacts directly (Received in original form September 3, 2003; accepted in final form January 21, 2005) Supported by grants from the National Institutes of Health (HL-63178), GlaxoSmithKline, and the Brewer Foundation. with free amine groups in proteins to form carbamate residues (14-16). CO 2 -dependent effects on the generation of reactive oxygen species and reactive nitrogen species as well as effects on ion channel conductivity have all been considered (17, 18).V...

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“…Recently, defects in post-translational glycosylation of membrane proteins have been shown to be causative factors in muscle-eye-brain disease, Fukuyama congenital muscular dystrophy, Walker-Warburg syndrome, congenital muscular dystrophy type 1C, and limb-girdle muscular dystrophy type 2I (6 -8). In most mammalian tissues, plasma membrane disruption is a common form of injury due to mechanical stress, and resealing of the damaged membrane is critical for cell survival (9,10). In skeletal muscle, disruptions of the membrane are more frequent due to the repeated lengthening and shortening of muscle cells during contraction (11).…”

mentioning

confidence: 99%

A Rostrocaudal Muscular Dystrophy Caused by a Defect in Choline Kinase Beta, the First Enzyme in Phosphatidylcholine Biosynthesis

Sher

Aoyama

Huebsch

et al. 2006

Journal of Biological Chemistry

109

102

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Muscular dystrophies include a diverse group of genetically heterogeneous disorders that together affect 1 in 2000 births worldwide. The diseases are characterized by progressive muscle weakness and wasting that lead to severe disability and often premature death. Rostrocaudal muscular dystrophy (rmd) is a new recessive mouse mutation that causes a rapidly progressive muscular dystrophy and a neonatal forelimb bone deformity. The rmd mutation is a 1.6-kb intragenic deletion within the choline kinase beta (Chkb) gene, resulting in a complete loss of CHKB protein and enzymatic activity. CHKB is one of two mammalian choline kinase (CHK) enzymes (␣ and ␤) that catalyze the phosphorylation of choline to phosphocholine in the biosynthesis of the major membrane phospholipid phosphatidylcholine. While mutant rmd mice show a dramatic decrease of CHK activity in all tissues, the dystrophy is only evident in skeletal muscle tissues in an unusual rostral-to-caudal gradient. Minor membrane disruption similar to dysferlinopathies suggest that membrane fusion defects may underlie this dystrophy, because severe membrane disruptions are not evident as determined by creatine kinase levels, Evans Blue infiltration, and unaltered levels of proteins in the dystrophin-glycoprotein complex. The rmd mutant mouse offers the first demonstration of a defect in a phospholipid biosynthetic enzyme causing muscular dystrophy, representing a unique model for understanding mechanisms of muscle degeneration.Muscular dystrophies are a variable class of more than 20 human disorders characterized by progressive muscle wasting and weakness resulting from myofiber degeneration and regeneration. Histologically, variation in myofiber size with centrally localized nuclei, fibrosis, and fatty infiltration are common features (1, 2). Despite their common pathologies, the genetic causes, severity, age of onset, and inheritance patterns vary widely among the dystrophies. The Muscular Dystrophy Association currently lists over 40 neuromuscular diseases as targets for its research programs and categorizes them by phenotypic characteristics such as age of onset, affected muscle groups, and inheritance pattern (Muscular Dystrophy Association, www.mdausa.org). In the last 10 years, the genetic mapping and identification of novel skeletal muscle genes, including cytoskeletal, cytosolic, nuclear membrane, sarcolemmal and extracellular matrix proteins, has dramatically changed this phenotype-based classification and provided clues as to the molecular basis of these disorders (3). What was once considered a single disease entity such as limb-girdle muscular dystrophy (LGMD) 4 has now been subdivided into seven different molecularly defined autosomal dominant (LGMD1A-1G) and ten autosomal recessive (LGMD2A-2J) diseases. Not surprisingly, many of these genes have converged to define pathways critical for the normal functioning and maintenance of skeletal muscles. The fact that many muscular dystrophy cases exist in which mutations to known dystrophy-causing genes have...

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The endomembrane requirement for cell surface repair

Cited by 136 publications

References 34 publications

Spatiotemporally controlled single cell sonoporation

Spatiotemporally controlled single cell sonoporation

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

A Rostrocaudal Muscular Dystrophy Caused by a Defect in Choline Kinase Beta, the First Enzyme in Phosphatidylcholine Biosynthesis

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