Depolymerisation and rearrangement of actin filaments during exocytosis in rat peritoneal mast cells: involvement of ryanodine-sensitive calcium stores

Guzman, Raul E.; Bolaños, Pura; Delgado, Alejandra; Rojas, Héctor; DiPolo, Reinaldo; Caputo, Carlo; Jaffe, E. H.

doi:10.1007/s00424-006-0177-z

Cited by 14 publications

(17 citation statements)

References 34 publications

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“…The longer t foot in presence of the fully active dynamin might indicate that the foot feature corresponds to the formation of the dynamin assembly and the initiation of GTPase activity, followed by the pore expansion. This concept, supported by several studies (Berberian et al 2009;Burgoyne et al 2001;Fulop et al 2008;Guzman et al 2007;Wang & Richards, 2011) suggests that the mechanochemical activity of dynamin is involved in exocytosis, and that this activity relies on its GTPase properties.…”

Section: Regulation Of Open and Closed Exocytosismentioning

confidence: 73%

The evidence for open and closed exocytosis as the primary release mechanism

Ren

Mellander

Keighron

et al. 2016

Quart. Rev. Biophys.

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Abstract. Exocytosis is the fundamental process by which cells communicate with each other. The events that lead up to the fusion of a vesicle loaded with chemical messenger with the cell membrane were the subject of a Nobel Prize in 2013. However, the processes occurring after the initial formation of a fusion pore are very much still in debate. The release of chemical messenger has traditionally been thought to occur through full distention of the vesicle membrane, hence assuming exocytosis to be all or none. In contrast to the all or none hypothesis, here we discuss the evidence that during exocytosis the vesicle-membrane pore opens to release only a portion of the transmitter content during exocytosis and then close again. This open and closed exocytosis is distinct from kiss-and-run exocytosis, in that it appears to be the main content released during regular exocytosis. The evidence for this partial release via open and closed exocytosis is presented considering primarily the quantitative evidence obtained with amperometry.1. An overview of exocytosis and endocytosis 2 2. Techniques to monitor exocytosis 5 2.1. Patch clamp 6 2.2. Amperometry 6 2.3. Patch amperometry 7 2.4. Cyclic voltammetry 7 2.5. Fluorescence microscopy imaging 83. Traditional models of exocytosis 94. Evidence where partial release during exocytosis appears to be dominant 11 4.1. The total content of a secretory vesicle is greater than the amount released 11 4.2. The majority of exocytotic events are followed by immediate endocytosis 12 4.3. Full distention of the vesicle may not be necessary for quantal release 13 4.4. A flickering fusion pore might regulate quantal release and vesicle recycling 15 4.5. Nanometer-sized pores can be seen as 'feet' associated with amperometric spikes 17 3. Release appears to be only a fraction of vesicle content in mammalian brains 23 7.4. Impact cytometry of adrenal cell vesicles shows a significantly larger catecholamine content then that released 23 7.5. Impact cytometry has been used to measure vesicle content in live cells and this quantity is greater than the amount released 23 7.6. Full distention of the vesicle is not necessary for the measured amperometric current during exocytotic release 23 7.7. Fast changes in cell environment alter the amount of messenger released 23 7.8. Patch amperometry measurements reveal a greater amount of release 23 7.9. Postspike 'feet' are observed with an amperometric spike 23Acknowledgements 24

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Section: Regulation Of Open and Closed Exocytosismentioning

confidence: 73%

The evidence for open and closed exocytosis as the primary release mechanism

Ren

Mellander

Keighron

et al. 2016

Quart. Rev. Biophys.

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“…19,23 Also, reorganization and depolymerization of the actin cytoskeleton is stimulated by C 48/80, leading to degranulation in mast cells. 24,25 It is possible that any of these mechanisms are involved in the modulation of the collagen lattice contraction observed in our experiments. In vivo, additional cell types such as neutrophils, macrophages, and endothelial cells probably contribute to generating signals affecting the collagen-remodeling properties of the fibroblasts.…”

Section: Discussionmentioning

confidence: 92%

The α11β1 Integrin Has a Mechanistic Role in Control of Interstitial Fluid Pressure and Edema Formation in Inflammation

Svendsen

Barczyk

Popova

et al. 2009

ATVB

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Objective-Collagen-binding integrins may be involved in controlling interstitial fluid pressure (Pif), transcapillary fluid flux, and tissue fluid volume. Our aim was to explore whether the newly discovered collagen binding ␣11␤1 integrin has a mechanistic role in inflammatory edema formation. Methods and Results-In collagen matrices seeded with a mixture of mast cells and fibroblasts, fibroblasts lacking the ␣11 integrin subunit (␣11 Ϫ/Ϫ ) contracted collagen gels less efficiently than control fibroblasts, suggesting that the ␣11␤1 integrin is able to mediate tensile force in connective tissues. In ␣11 Ϫ/Ϫ mice, control Pif in skin did not differ from the pressure found in wild-type mice. Whereas a reduction in Pif was found in control mice after inducing inflammation, thereby contributing to fluid extravasation and edema formation, such a reduction was not seen in ␣11 Ϫ/Ϫ mice. That this effect is mediated through the extracellular compartment is suggested by a similar plasma protein extravasation ratio in ␣11Ϫ/Ϫ and wild-type mice. Conclusions-Our data suggest that ␣11␤1 integrins on dermal fibroblasts mediate collagen lattice remodeling and have a mechanistic role in controlling Pif in inflammation and thereby fluid extravasation and edema formation in vivo. Key Words: collagen Ⅲ endothelium Ⅲ extracellular matrix Ⅲ genetically altered mice Ⅲ microcirculation F luid flux across the capillaries is governed by hydrostatic and colloid osmotic pressure gradients between plasma and interstitium. Edema (ie, extravascular fluid accumulation in the tissue) is one of the key features of inflammation and is the result of increased transcapillary fluid transport in this condition. During inflammation there is an increased capillary leakage, but also initially a rapid decrease in the hydrostatic pressure outside the capillary, the interstitial fluid pressure (Pif), which is quantitatively more important than increased capillary permeability as a driving force in the initial phase of edema generation. 1,2 Traditionally, cells are not included in the interstitium, defined as the extracellular compartment between the blood vessels and lymphatics of a tissue. 3,4 In recent studies, however, we have shown an active role of the interstitium in edema generation during inflammation (reviewed in 2 ), and in the present context we include cells (ie, fibroblasts) when addressing the mechanisms for edema generation. Furthermore, our studies have suggested a role for integrins in controlling interstitial fluid volume (Vif) by their ability to modulate force from the cytoskeleton inside the cells to the structural proteins (ie, collagens) of the extracellular matrix outside the cell. The normal fluid homeostasis is dependent on functioning collagen-binding integrins, and the result of perturbed integrin function can be edema. 2,5,6 There are four collagen-binding integrins: ␣1␤1, ␣2␤1, ␣10␤1 and ␣11␤1, and in previous studies we have shown a role for ␣2␤1 in control of Vif. 6,7 The ␣11␤1 integrin has, similar to the ␣2␤1 integr...

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“…[40],[41] In this case, a system constituted uniquely of the SNARE proteins, the cell membrane and the actin cytoskeleton would mostly lead to hastily closing fusion pores. The mechanochemical activity of the active dynamin complex would, in this case, help to counteract pressure induced by the cytoskeleton on the pore and lead to larger peaks than in the absence of the GTPase activity of dynamin.…”

Section: Resultsmentioning

confidence: 99%

Amperometric Measurements at Cells Support a Role for Dynamin in the Dilation of the Fusion Pore during Exocytosis

Trouillon

Ewing

2013

ChemPhysChem

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Dynamin is a GTPase mechanochemical enzyme involved in the late steps of endocytosis, where it separates the endocytotic vesicle from the cell membrane. However, recent reports have emphasized its role in exocytosis. In this case, dynamin may contribute to the control of the exocytotic pore, thus suggesting a direct control on the efflux of neurotransmitters. Dynasore, a selective inhibitor of the GTPase activity of dynamin, was used to investigate the role of dynamin in exocytosis. Exocytosis was analyzed by amperometry, thus revealing that dynasore inhibits exocytosis in a dose-dependent manner. Analysis of the exocytotic peaks showed that the inhibition of the GTPase activity of dynamin led to shorter, smaller events. This observation, together with the rapid effect of dynasore, suggests that the blocking of the GTPase induces the formation of a more narrow and short-lived fusion pore. These results suggest that the GTPase properties of dynamin are involved in the duration and kinetics of exocytotic release. Interestingly, and in strong contrast with its role in endocytosis, the mechanochemical properties of dynamin appear to contribute to the dilation and stability of the pore during exocytosis.

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Depolymerisation and rearrangement of actin filaments during exocytosis in rat peritoneal mast cells: involvement of ryanodine-sensitive calcium stores

Cited by 14 publications

References 34 publications

The evidence for open and closed exocytosis as the primary release mechanism

The evidence for open and closed exocytosis as the primary release mechanism

The α11β1 Integrin Has a Mechanistic Role in Control of Interstitial Fluid Pressure and Edema Formation in Inflammation

Amperometric Measurements at Cells Support a Role for Dynamin in the Dilation of the Fusion Pore during Exocytosis

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