Massive calcium–activated endocytosis without involvement of classical endocytic proteins

Lariccia, Vincenzo; Fine, Michael J.; Magi, Simona; Lin, Mei-Jung; Yaradanakul, Alp; Llaguno, Marc C.; Hilgemann, Donald W.

doi:10.1085/jgp.2010104681376c

Cited by 20 publications

(51 citation statements)

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“…The calcium influx mediated by those ROS is overcompensated by potassium efflux via BKCa channels, resulting in hyperpolarization of the cell membrane [57]. Moreover, calcium influx is shown to stimulate endocytosis [149]. (C) The microstreamings generated by stably cavitating bubbles and the corresponding shear stresses can deform the cell membrane.…”

Section: Figure 3 Biological Effects Of Stably and Inertial Cavitatimentioning

confidence: 99%

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Understanding ultrasound induced sonoporation: Definitions and underlying mechanisms

Lentacker

Cock

Deckers

et al. 2014

Advanced Drug Delivery Reviews

672

592

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In the past two decades, research has underlined the potential of ultrasound and microbubbles to enhance drug delivery. However, there is less consensus on the biophysical and biological mechanisms leading to this enhanced delivery. Sonoporation, i.e. the formation of temporary pores in the cell membrane, as well as enhanced endocytosis is reported. Because of the variety of ultrasound settings used -and corresponding microbubble behavior, a clear overview is missing. Therefore, in this review, the mechanisms contributing to sonoporation are categorized according to three ultrasound settings: i) low intensity ultrasound leading to stable cavitation of microbubbles, ii) high intensity ultrasound leading to inertial cavitation with microbubble collapse, and iii) ultrasound application in the absence of microbubbles. Using low intensity ultrasound, the endocytotic uptake of several drugs could be stimulated, while short but intense ultrasound pulses can be applied to induce pore formation and the direct cytoplasmic uptake of drugs. Ultrasound intensities may be adapted to create pore sizes correlating with drug size. Small molecules are able to diffuse passively through small pores created by low intensity ultrasound treatment. However, delivery of larger drugs such as nanoparticles and gene complexes, will require higher ultrasound intensities in order to allow direct cytoplasmic entry.2

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Section: Figure 3 Biological Effects Of Stably and Inertial Cavitatimentioning

confidence: 99%

“…These cell membrane domains can spontaneously vesiculate and form endocytic vesicles under the influence of Ca 2+ [149]. This mechanism might be important in reference to the calcium waves which move from the sonoporated cells to adjacent cells [35,36,59,150].…”

Section: +mentioning

confidence: 99%

Understanding ultrasound induced sonoporation: Definitions and underlying mechanisms

Lentacker

Cock

Deckers

et al. 2014

Advanced Drug Delivery Reviews

672

592

View full text Add to dashboard Cite

show abstract

“…Although there is evidence that cytosolic Ca 2þ is needed for endocytosis, elevations of cytosolic Ca 2þ above its physiological levels are not essential for this process (Ceccarelli and Hurlbut 1980;Wu and Betz 1996;Gad et al 1998;Balaji et al 2008). However, a transient elevation in cytosolic Ca 2þ triggers various forms of clathrin-independent endocytosis in a variety of cell types (Artalejo et al 1995;Neves et al 2001;Wu et al 2009;Lariccia et al 2010), and a stimulus-dependent cytosolic Ca 2þ increase may also play a role in bulk endocytosis at synapses. Furthermore, a sustained increase in cytosolic Ca 2þ accelerates endocytosis (Sankaranarayanan and Ryan 2000Ryan , 2001Wu et al 2005;Balaji et al 2008).…”

Section: Synaptic Vesicle Endocytosismentioning

confidence: 99%

Synaptic Vesicle Endocytosis

Saheki

Camilli

2012

Cold Spring Harbor Perspectives in Biology

377

432

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Neurons can sustain high rates of synaptic transmission without exhausting their supply of synaptic vesicles. This property relies on a highly efficient local endocytic recycling of synaptic vesicle membranes, which can be reused for hundreds, possibly thousands, of exoendocytic cycles. Morphological, physiological, molecular, and genetic studies over the last four decades have provided insight into the membrane traffic reactions that govern this recycling and its regulation. These studies have shown that synaptic vesicle endocytosis capitalizes on fundamental and general endocytic mechanisms but also involves neuron-specific adaptations of such mechanisms. Thus, investigations of these processes have advanced not only the field of synaptic transmission but also, more generally, the field of endocytosis. This article summarizes current information on synaptic vesicle endocytosis with an emphasis on the underlying molecular mechanisms and with a special focus on clathrin-mediated endocytosis, the predominant pathway of synaptic vesicle protein internalization.

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“…Massive, calcium-activated endocytosis, which did not involve any of the classical endocytic proteins (clathrin, dynamin, the actin cytoskeleton), has recently been described [17]. This type of ''excessive'' endocytosis, which might affect up to 25% of a cell's surface [17] reflects the formation of ceramide domains that develop high inward curvature and undergo spontaneous budding [41].…”

Section: Discussionmentioning

confidence: 99%

“…Massive, calcium-activated endocytosis of the plasma membrane without involvement of classical endocytic proteins is a recently described phenomenon and is closely associated with the formation of ceramide during cellular stress [17][18][19][20]. We have investigated interorganellar membrane contacts during this process.…”

Section: Introductionmentioning

confidence: 99%

The targeting of plasmalemmal ceramide to mitochondria during apoptosis

Babiychuk

Monastyrskaya

Draeger

2010

Chemistry and Physics of Lipids

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Ceramide is a key lipid mediator of cellular processes such as differentiation, proliferation, growth arrest and apoptosis. During apoptosis, ceramide is produced within the plasma membrane. Although recent data suggest that the generation of intracellular ceramide increases mitochondrial permeability, the source of mitochondrial ceramide remains unknown. Here, we determine whether a stress-mediated plasmalemmal pool of ceramide might become available to the mitochondria of apoptotic cells. We have previously established annexin A1-a member of a family of Ca 2+ and membrane-binding proteins-to be a marker of ceramide platforms. Using fluorescently tagged annexin A1, we show that, upon its generation within the plasma membrane, ceramide self-associates into platforms that subsequently invaginate and fuse with mitochondria. An accumulation of ceramide within the mitochondria of apoptotic cells was also confirmed using a ceramide-specific antibody. Electron microscopic tomography confirmed that upon the formation of ceramide platforms, the invaginated regions of the plasma membrane extend deep into the cytoplasm forming direct physical contacts with mitochondrial outer membranes. Ceramide might thus be directly transferred from the plasma membrane to the mitochondrial outer membrane. It is conceivable that this ''kiss-of-death'' increases the permeability of the mitochondrial outer membrane thereby triggering apoptosis.

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Massive calcium–activated endocytosis without involvement of classical endocytic proteins

Abstract: In this article, the primary institutional affiliation of Drs. Vincenzo Lariccia and Simona Magi should have been given as:

Cited by 20 publications

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Understanding ultrasound induced sonoporation: Definitions and underlying mechanisms

Understanding ultrasound induced sonoporation: Definitions and underlying mechanisms

Synaptic Vesicle Endocytosis

The targeting of plasmalemmal ceramide to mitochondria during apoptosis

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