A membrane potential-sensitive dye for vascular smooth muscle cells assays

Sguilla, F.S.; Tedesco, Antônio Cláudio; Bendhack, Lusiane Maria

doi:10.1016/s0006-291x(02)02973-x

Cited by 16 publications

(13 citation statements)

References 27 publications

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“…A similar depolarization was found by flow-cytometric measurement, e.g., in rat spinal cord cells after treatment with batrachotoxin [11,12]. The analysis of the depolarized membrane potential is a useful technique to study ion channelmediated changes in membrane potential due to the influence of a pharmaceutical [1,24]. In our future work we want to focus on mibefradil's mode of functioning, especially on the inhibition of T-type calcium channels in hLEC, which we were able to identify.…”

Section: Discussionsupporting

confidence: 63%

Induction of apoptosis by the calcium antagonist mibefradil correlates with depolarization of the membrane potential and decreased integrin expression in human lens epithelial cells

Nebe

Kunz

Peters

et al. 2004

Graefe's Arch Clin Exp Ophthalmol

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Section: Discussionsupporting

confidence: 63%

Induction of apoptosis by the calcium antagonist mibefradil correlates with depolarization of the membrane potential and decreased integrin expression in human lens epithelial cells

Nebe

Kunz

Peters

et al. 2004

Graefe's Arch Clin Exp Ophthalmol

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“…Membrane potential was determined using DiBAC 4 (5) fluorescent dye 35, 36. Synaptosomes were resuspended into saline A with glucose21 to a final protein concentration of 2 mg mL −1 and incubated with the appropriate pretreatments or DMSO.…”

Section: Methodsmentioning

confidence: 99%

Neurotoxic implications of the agonistic action of CS‐syndrome pyrethroids on the N‐type Ca_v2.2 calcium channel

Clark

Symington

2008

Pest Management Science

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BACKGROUND: Cismethrin (T-syndrome) and deltamethrin (CS-syndrome) pyrethroids have been previously shown to increase membrane depolarization and calcium influx, but only deltamethrin increased Ca 2+ -dependent neurotransmitter release from rat brain synaptosomes. Deltamethrin's action was blocked by ω-conotoxin GVIA, delineating a separate action at N-type Ca v 2.2 channels that is consistent with the in vivo release of neurotransmitter. It is hypothesized that other CS-syndrome pyrethroids will elicit similar actions at presynaptic nerve terminals.RESULTS: Nine additional pyrethroids were similarly examined, and these data were used in a cluster analysis. CS-syndrome pyrethroids that possessed α-cyano groups, cypermethrin, deltamethrin and esfenvalerate, all caused Ca 2+ influx and neurotransmitter release and clustered with two other α-cyano pyrethroids, cyfluthrin and cyhalothrin, that shared these same actions. T-syndrome pyrethroids, bioallethrin, cismethrin and fenpropathrin, did not share these actions and clustered with two non-α-cyano pyrethroids, tefluthin and bifenthrin, which likewise did not elicit these actions. Deltamethrin reduced peak current of heterologously expressed wild-type Ca v 2.2, increased peak current of T422E Ca v 2.2 and was 20-fold more potent on T422E Ca v 2.2 than on wild-type channels, indicating that the permanently phosphorylated form of Ca v 2.2 is the preferred target. CONCLUSIONS: Ca v 2.2 is directly modified by deltamethrin, but the resulting perturbation is dependent upon its phosphorylation state. The present findings may provide a partial explanation for the different toxic syndromes produced by these structurally distinct pyrethroids.

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“…7). Bisoxonol dyes have been extensively used to optically determine the plasma membrane potential of various cell types, including endothelial cells (DallAsta et al, 1997;He and Curry, 1995;Sguilla et al, 2003;Simon et al, 2009). They belong to the slowresponse voltage-dependent dyes and distribute between the extracellular space and the cell cytosol in a manner dependent on the magnitude of the electrical plasma membrane potential difference.…”

Section: Simultaneous Afm Stiffness-and Fluorescence-based Potential mentioning

confidence: 99%

Membrane potential depolarization decreases the stiffness of vascular endothelial cells

Callies

Fels

Liashkovich

et al. 2011

Journal of Cell Science

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The stiffness of vascular endothelial cells is crucial to mechanically withstand blood flow and, at the same time, to control deformation-dependent nitric oxide release. However, the regulation of mechanical stiffness is not yet understood. There is evidence that a possible regulator is the electrical plasma membrane potential difference. Using a novel technique that combines fluorescence-based membrane potential recordings with atomic force microscopy (AFM)-based stiffness measurements, the present study shows that membrane depolarization is associated with a decrease in the stiffness of endothelial cells. Three different depolarization protocols were applied, all of which led to a similar and significant decrease in cell stiffness, independently of changes in cell volume. Moreover, experiments using the actin-destabilizing agent cytochalasin D indicated that depolarization acts by affecting the cortical actin cytoskeleton. A model is proposed whereby a change of the electrical field across the plasma membrane is directly sensed by the submembranous actin network, regulating the actin polymerization:depolymerization ratio and thus cell stiffness. This depolarization-induced decrease in the stiffness of endothelial cells could play a role in flow-mediated nitric-oxide-dependent vasodilation.

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A membrane potential-sensitive dye for vascular smooth muscle cells assays

Cited by 16 publications

References 27 publications

Induction of apoptosis by the calcium antagonist mibefradil correlates with depolarization of the membrane potential and decreased integrin expression in human lens epithelial cells

Induction of apoptosis by the calcium antagonist mibefradil correlates with depolarization of the membrane potential and decreased integrin expression in human lens epithelial cells

Neurotoxic implications of the agonistic action of CS‐syndrome pyrethroids on the N‐type Ca_v2.2 calcium channel

Membrane potential depolarization decreases the stiffness of vascular endothelial cells

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A membrane potential-sensitive dye for vascular smooth muscle cells assays

Cited by 16 publications

References 27 publications

Induction of apoptosis by the calcium antagonist mibefradil correlates with depolarization of the membrane potential and decreased integrin expression in human lens epithelial cells

Induction of apoptosis by the calcium antagonist mibefradil correlates with depolarization of the membrane potential and decreased integrin expression in human lens epithelial cells

Neurotoxic implications of the agonistic action of CS‐syndrome pyrethroids on the N‐type Cav2.2 calcium channel

Membrane potential depolarization decreases the stiffness of vascular endothelial cells

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Neurotoxic implications of the agonistic action of CS‐syndrome pyrethroids on the N‐type Ca_v2.2 calcium channel