Dealing with damage: Plasma membrane repair mechanisms

Draeger, Annette; Schoenauer, Roman; Atanassoff, Alexander P.; Wolfmeier, Heidi; Babiychuk, Eduard B.

doi:10.1016/j.biochi.2014.08.008

Cited by 62 publications

(69 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such a “clot” mechanism, referred to as a surface precipitation reaction, was actually described in one of the very early studies of plasma membrane repair [1]. This proposed mechanism is very consistent with previous imaging studies showing dense annexin clusters associated with wound sites, and with the suggestion that these protein aggregates prevent cytosol loss while allowing the more definitive membrane-mediated repair to proceed [24,43]. Future studies should clarify additional intriguing aspects of the mechanism by which annexins facilitate plasma membrane repair, including their interaction with S100A11, a protein up-regulated in metastatic tumors that was suggested to facilitate resealing by stimulating cortical actin polymerization [52].…”

Section: Ca2+-activated Proteins Implicated In Plasma Membrane Repsupporting

confidence: 79%

“…Fusion of lysosomes with the plasma membrane in response to injury has now been observed in several laboratories with different cell types, including cells exposed to pathogens, wounded mechanically or permeabilized by pore-forming proteins such as bacterial toxins or perforin from cytotoxic lymphocytes (CTL) [14–20]. Given the consistency by which lysosomal exocytosis is observed in wounded cells, it has been increasingly suggested that lysosomes are the main intracellular organelle that originates the “patch” responsible for membrane resealing [18,21–24]. …”

Section: It Is Time To Revisit the “Patch” Hypothesis - The Abundamentioning

confidence: 99%

“…As discussed elsewhere [37], disruption of the cortical actin cytoskeleton at the site of Ca 2+ influx triggers the transient formation of large plasma membrane blebs, which retract back into the cell body within a few seconds, as the cell reseals [38]. Thus, additional studies are needed to clarify whether plasma membrane blebbing and shedding are a phenomenon that occurs in parallel with other wound repair mechanisms, or if it is directly responsible for lesion removal [20,24]. It will be important to determine if there is massive membrane shedding specifically from wounded cells undergoing resealing, if this occurs at a rate compatible with the rapid kinetics of plasma membrane repair, and whether this mechanism only applies to wounds of a certain size range.…”

Section: Repair Of Large and Small Wounds - Similarities And Diffementioning

confidence: 99%

“…These results suggest an additional level of complexity in the resealing of larger, irregular wounds, which may require the highly localized, spatially regulated exocytic events coupled to interactions with the actin cytoskeleton that are characteristic of the exocyst complex [41]. This is a very interesting possibility, because it can explain the apparent contradiction regarding involvement of the actin cytoskeleton in the resealing of certain forms of wounds, but not others [24,42]. …”

Section: Repair Of Large and Small Wounds - Similarities And Diffementioning

confidence: 99%

See 3 more Smart Citations

Above the fray: Surface remodeling by secreted lysosomal enzymes leads to endocytosis-mediated plasma membrane repair

Andrews

Corrotte

Castro-Gomes

2015

Seminars in Cell & Developmental Biology

View full text Add to dashboard Cite

The study of plasma membrane repair is coming of age. Mirroring human adolescence, the field shows at the same time signs of maturity and significant uncertainty, confusion and skepticism. Here we discuss concepts that emerged from experimental data over the years, some of which are solidly established while others are still subject to different interpretations. The firmly established concepts include the critical requirement for Ca2+ in wound repair, and the role of rapid exocytosis of intracellular vesicles. Lysosomes are being increasingly recognized as the major vesicles involved in injury-induced exocytosis in many cell types, as a growing number of laboratories detect markers for these organelles on the cell surface and lysosomal hydrolases in the supernatant of wounded cells. The more recent observation of massive endocytosis following Ca2+-triggered exocytosis initially came as a surprise, but this finding is also being increasingly reported by different groups, shifting the discussion to the mechanisms by which endocytosis promotes repair, and whether it operates or not in parallel with the shedding of membrane blebs. We discuss how the abundant intracellular vesicles that undergo homotypic fusion close to wound sites, previously interpreted as exocytic membrane patches, actually acquire extracellular tracers demonstrating their endocytic origin. We also suggest that an initial, temporary patch that prevents cyto-sol loss until the bilayer is restored might result not from vesicular fusion, but from rapid Ca2+-dependent crosslinking and aggregation of cytosolic proteins. Finally, we propose that cell surface remodeling, orchestrated by the extracellular release of lysosomal hydrolases and perhaps also cytosolic molecules, may represent a key aspect of the plasma membrane repair mechanism that has received little attention so far.

show abstract

Section: Ca2+-activated Proteins Implicated In Plasma Membrane Repsupporting

confidence: 79%

Section: It Is Time To Revisit the “Patch” Hypothesis - The Abundamentioning

confidence: 99%

Section: Repair Of Large and Small Wounds - Similarities And Diffementioning

confidence: 99%

Section: Repair Of Large and Small Wounds - Similarities And Diffementioning

confidence: 99%

See 2 more Smart Citations

Above the fray: Surface remodeling by secreted lysosomal enzymes leads to endocytosis-mediated plasma membrane repair

Andrews

Corrotte

Castro-Gomes

2015

Seminars in Cell & Developmental Biology

View full text Add to dashboard Cite

show abstract

“…Cell models have implicated several annexins, including AnxA6, in membrane repair (Skrahina et al, 2008;Draeger et al, 2014). In zebrafish, AnxA6 is rapidly recruited to damaged sarcolemma and may cooperate with dysferlin to repair membrane lesions.…”

Section: Anxa6 Ko Micementioning

confidence: 99%

Annexins – insights from knockout mice

Grewal

Wason

Enrich

et al. 2016

Biological Chemistry

View full text Add to dashboard Cite

Annexins are a highly conserved protein family that bind to phospholipids in a calcium (Ca 2+ ) -dependent manner. Studies with purified annexins, as well as overexpression and knockdown approaches identified multiple functions predominantly linked to their dynamic and reversible membrane binding behavior. However, most annexins are found at multiple locations and interact with numerous proteins. Furthermore, similar membrane binding characteristics, overlapping localizations and shared interaction partners have complicated identification of their precise functions. To gain insight into annexin function in vivo, mouse models deficient of annexin A1 (AnxA1), A2, A4, A5, A6 and A7 have been generated. Interestingly, with the exception of one study, all mice strains lacking one or even two annexins are viable and develop normally. This suggested redundancy within annexins, but examining these knockout (KO) strains under stress conditions revealed striking phenotypes, identifying underlying mechanisms specific for individual annexins, often supporting Ca 2+ homeostasis and membrane transport as central for annexin biology. Conversely, mice lacking AnxA1 or A2 show extracellular functions relevant in health and disease that appear independent of membrane trafficking or Ca 2+ signaling. This review will summarize the mechanistic insights gained from studies utilizing mouse models lacking members of the annexin family.

show abstract

Toxicological Analysis UsingDNAFragmentation

Basnakian

Braman

Yin

et al. 2017

Encyclopedia of Analytical Chemistry

View full text Add to dashboard Cite

Toxicological analysis relies on the measurement of cell death. DNA fragmentation is the preferential method in cell death assessment because it measures irreversible stage of cell death, and it is universal to all mechanisms of cell death. DNA fragmentation is provided by a group of nine cytotoxic DNases/endonucleases, cumulative activity of which is sufficient to eventually destroy all cellular DNAs to potentially reusable mononucleotides. Of all the methods for measuring DNA fragmentation, the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay seems to be the best in satisfying the toxicology assessment because it is simple, quantitative, based on individual cell measurements, and is not destructive to the cells. The latter allows it to combine with quantitative immunocytochemistry and other histology and genetic techniques to perform mechanistic studies.

show abstract

Dealing with damage: Plasma membrane repair mechanisms

Cited by 62 publications

References 75 publications

Above the fray: Surface remodeling by secreted lysosomal enzymes leads to endocytosis-mediated plasma membrane repair

Above the fray: Surface remodeling by secreted lysosomal enzymes leads to endocytosis-mediated plasma membrane repair

Annexins – insights from knockout mice

Toxicological Analysis UsingDNAFragmentation

Contact Info

Product

Resources

About