Cytoskeletal modulation of the response to mechanical stimulation in human vascular endothelial cells

Oike, Masahiro; Schwarz, Gero; Sehrer, J; Jost, Matthias; Gerke, Volker; Weber, Klaus; Droogmans, Guy; Nilius, Bernd

doi:10.1007/bf00374579

Cited by 48 publications

(35 citation statements)

References 25 publications

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“…The similar results in other cells have been reported. In Blymphocyte, no I (Cl,swell) was recorded after F-actin integrity was disrupted by application of CB [9]. Sup-pression of RVD by CB was also observed in cultured PC12 cells [24], Necturus maculosus gallbladder epithelial cells [8] and isolated axons of the green crab Carcinus maenas [25].…”

Section: Discussionmentioning

confidence: 94%

“…Therefore, an intact F-actin network was considered to be critical for normal volume regulatory response in these cells. However, I (Cl,swell) in human endothelial cells was not affected by F-actin disruption [9], and F-actin disassembly in B-lymphocyte was not essential for activation of I (Cl,swell) [10]. So, the functional relationship between F-actin and I (Cl,swell) is still not clear.…”

Section: Introductionmentioning

confidence: 98%

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Regulation of swelling-activated chloride channels in embryonic chick heart cells

et al. 2003

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Swelling-activated Cl − currents, I (Cl,swell) , were measured during hyposmotic shock in white Leghorn embryonic chick heart cells using the whole-cell recording of patch-clamp technique. Genistein, an inhibitor of protein tyrosine kinase (PTK), suppressed I (Cl,swell) . Under isosmotic condition phorbol 12-myristate 13-acetate (PMA), an activator of PKC, elicited the Cl − current similar to that in hyposmotic solution, whereas hyposmotic shock did not elicit I (Cl,swell) in chelerythrine chloride(an inhibitor of PKC)-treated cells. Confocal microscopy experiments using FITC-phalloidin as a fluorescent label of F-actin showed that the actin network was moved from cortical region of the cell to the center after hyposmotic shock as compared with the image under isosmotic condition. When the cells were treated with cytochalasin B (CB) or cytochalasin D (CD) under isosmotic condition the disruption of the F-actin integrity was observed, and I (Cl,swell) was not elicited. With combination treatment of CB with PMA, hyposmotic solution could not elicited I (Cl,swell) . The results suggested that the role of PTK, probably receptor tyrosine kinase, for regulation of I (Cl,swell) appeared to be at upstream site related to the role of F-actin. Then PKC signal pathway was activated somehow and finally change in the polymerization state of cytoskeleton led to activate the swelling-activated Cl − channels. These results demonstrate clearly that PTK, PKC and F-actin are important factors for regulation of I (Cl, swell) , in embryonic chick heart cells as compared with often controversial results reported in different cell types.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 98%

Regulation of swelling-activated chloride channels in embryonic chick heart cells

et al. 2003

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“…Peptides-The peptide comprising the N-terminal 14 amino acids of bovine annexin II (STVHEILCKLSLEG) (25) and the L7E mutant version (STVHEIECKLSLEG) were synthesized on an automated sequencer (model 9050; Milligen). To verify the purity a small aliquot of the preparation was deprotected and subjected to automated sequence analysis.…”

Section: Methodsmentioning

confidence: 99%

Annexin II Modulates Volume-activated Chloride Currents in Vascular Endothelial Cells

Nilius

Gerke

Prenen

et al. 1996

Journal of Biological Chemistry

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The membrane-associated, microfilament-binding protein annexin II is abundantly expressed in endothelial cells from calf pulmonary artery (CPAE cells). We have analyzed its role in the regulation of volume-activated chloride currents (I Cl, vol ) by loading the cells via the patch pipette with a peptide comprising the N-terminal 14 residues of annexin II. This sequence harbors the binding site for the intracellular annexin II ligand, p11, and the peptide interferes with the annexin II-p11 complex formation. Loading of a CPAE cell with this peptide caused a gradual decrease in the amplitude of I Cl, vol during repetitive stimulations with a 28% hypotonic extracellular solution. This run down of the current was virtually absent in untreated cells and in cells that were loaded with a mutated 14-amino acid peptide, which has a single amino acid replacement known to result in a more than 1000 times reduced affinity for binding to p11. We conclude that annexin II-p11 complex formation is either directly or indirectly involved in the activation of I Cl, vol in endothelial cells.

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“…2-4). Particularly, swelling-induced rearrangements of cytoskeletal elements regulate the opening of VRAC in some cell types (25)(26)(27), whereas a complete disruption of the cytoskeleton did not affect activation of I Cl,swell in endothelial cells (28).…”

mentioning

confidence: 91%

Reduced intracellular ionic strength as the initial trigger for activation of endothelial volume-regulated anion channels

Voets

Droogmans

Raskin

et al. 1999

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

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130

107

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Most mammalian cell types, including endothelial cells, respond to cell swelling by activating a Cl ؊ current termed I Cl,swell , but it is not known how the physical stimulus of cell swelling is transferred to the channels underlying I Cl,swell . We have investigated the precise relation between cell volume and I Cl,swell in endothelial cells by performing whole-cell current recordings while continuously monitoring cell thickness (T c ) as a measure for cell volume. The time course of T c was accurately predicted by a theoretical model that describes volume changes of patch-clamped cells in response to changes in the extracellular osmolality (OSM o ). This model also predicts significant changes in intracellular ionic strength (⌫ i ) when OSM o is altered. Under all experimental conditions I Cl,swell closely followed the changes in ⌫ i , whereas I Cl,swell and cell volume were often found to change independently. These results do not support the hypothesis that ⌫ i regulates the volume set point for activation of I Cl,swell . Instead, they are in complete agreement with a model in which a decrease of ⌫ i rather than an increase in cell volume is the initial trigger for activation of I Cl,swell .All living cells are programmed to activate a series of cellular processes to counter the harmful effects of cell swelling. One of the first detectable effects of cell swelling in most vertebrate cells is an increase in the plasma membrane permeability to anions, through the opening of anion channels (1). Although different types of swelling-activated anion currents have been functionally described, one phenotype seems to be predominant. This outwardly rectifying current, which under normal conditions is mainly carried by Cl Ϫ , has been termed I Cl,swell for swelling-activated Cl Ϫ current, and the underlying channel has been termed VRAC for volume-regulated anion channel. The biophysical and pharmacological properties of I Cl,swell ͞VRAC have been extensively studied (for recent reviews, see refs. 2-4), but the precise activation mechanism of I Cl,swell is still not resolved. Particularly, it remains unclear how the cell ''senses'' changes in its volume and translates this physical stimulus into the opening of VRAC.Hypotonicity-induced cell swelling is accompanied by a dilution of the intracellular medium, resulting in a decrease of ⌫ i , the intracellular ionic strength. Interestingly, it was recently shown that ⌫ i modulates I Cl,swell , independent of the molecular nature of the intracellular ions. A model was proposed in which ⌫ i regulates the volume set point for activation of VRAC, by modulating a putative ''volume sensor '' (5-7).In the present study we tested this model by investigating the relation between cell volume, ⌫ i , and I Cl,swell in endothelial cells. To this end, we set up a combined system that enables the simultaneous measurement of whole-cell currents and cell thickness (T c ). A theoretical model was developed that accurately predicts the osmotically induced volume changes and the conco...

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Cytoskeletal modulation of the response to mechanical stimulation in human vascular endothelial cells

Cited by 48 publications

References 25 publications

Regulation of swelling-activated chloride channels in embryonic chick heart cells

Regulation of swelling-activated chloride channels in embryonic chick heart cells

Annexin II Modulates Volume-activated Chloride Currents in Vascular Endothelial Cells

Reduced intracellular ionic strength as the initial trigger for activation of endothelial volume-regulated anion channels

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