Membrane potential depolarization decreases the stiffness of vascular endothelial cells

Callies, Chiara; Fels, Johannes; Liashkovich, Ivan; Kliche, Katrin; Jeggle, Pia; Kusche-Vihrog, Kristina; Oberleithner, Hans

doi:10.1242/jcs.084657

Cited by 80 publications

(84 citation statements)

References 66 publications

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“…We also found that Na V 1.5 function in cancer cells enhanced Src kinase activity and Y421 cortactin phosphorylation, which could contribute to the acquisition of an aggressive phenotype. Although the mechanism has not yet been elucidated, this could be in line with the observation that membrane depolarisation regulates the actin polymerisation:actin depolymerisation ratio and thus, the F-actin network directly under the plasmalemma (Callies et al, 2011). This effect on actin polymerisation could also be dependent on the interaction of actin with NHE-1 through the association with actin-binding proteins of the ERM (ezrin, radixin and moesin) family (Baumgartner et al, 2004;Cardone et al, 2005).…”

Section: Resultssupporting

confidence: 56%

NaV1.5 sodium channels allosterically regulate the NHE-1 exchanger and promote breast cancer cell invadopodial activity

Brisson

Driffort

Benoist

et al. 2013

Journal of Cell Science

135

153

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SummaryThe degradation of the extracellular matrix by cancer cells represents an essential step in metastatic progression and this is performed by cancer cell structures called invadopodia. Na V 1.5 (also known as SCN5A) Na + channels are overexpressed in breast cancer tumours and are associated with metastatic occurrence. It has been previously shown that Na V 1.5 activity enhances breast cancer cell invasiveness through perimembrane acidification and subsequent degradation of the extracellular matrix by cysteine cathepsins. Here, we show that Na V 1.5 colocalises with Na + /H + exchanger type 1 (NHE-1) and caveolin-1 at the sites of matrix remodelling in invadopodia of MDA-MB-231 breast cancer cells. NHE-1, Na V 1.5 and caveolin-1 co-immunoprecipitated, which indicates a close association between these proteins. We found that the expression of Na V 1.5 was responsible for the allosteric modulation of NHE-1, rendering it more active at the intracellular pH range of 6.4-7; thus, it potentially extrudes more protons into the extracellular space. Furthermore, Na V 1.5 expression increased Src kinase activity and the phosphorylation (Y421) of the actin-nucleation-promoting factor cortactin, modified F-actin polymerisation and promoted the acquisition of an invasive morphology in these cells. Taken together, our study suggests that Na V 1.5 is a central regulator of invadopodia formation and activity in breast cancer cells.

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Section: Resultssupporting

confidence: 56%

NaV1.5 sodium channels allosterically regulate the NHE-1 exchanger and promote breast cancer cell invadopodial activity

Brisson

Driffort

Benoist

et al. 2013

Journal of Cell Science

135

153

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“…When QTc interval is prolonged, it may become a risk factor for ventricular tachyarrhythmias and sudden death. This condition can arise as a genetic syndrome, or may be as a side effect of certain medications, but, an unusually short QTc can be seen in severe hypercalcemia (29,30,31,32). In this study, all the tested doses brought about an increase in QT and QTc interval.…”

Section: Discussionmentioning

confidence: 99%

Cardiotoxicity Study of the Aqueous Extract of Corn Silk in Rats

Adedapo

Babarinsa

Oyagbemi

et al. 2016

Macedonian Veterinary Review

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Original Scientific Article Mac Vet Rev 2016; 39 (1): 43-49 In the ear of corn there are silky strands which run its length and these strands are known as corn silks. Folk remedies show that the corn silks have been used as an oral antidiabetic agent in China for many years and as herbal tea in other world nations for the amelioration of urinary tract infection. The extract is being assessed for safety in this study using histopathological changes, as well as an electrocardiogram (ECG). Graded doses (200, 400 and 800 mg/kg) of aqueous CS extract were administered to rats for seven days. The fourth group which served as control received 3 ml/kg dose of distilled water. On the eighth day, ECG was evaluated in ketamine/xylazine-induced anaesthesia in rats to determine changes in the heart rate, P-wave duration, P-R interval, R-amplitude, QRS duration, QT interval and QTc. Hearts from the experimental animals were collected for histopathological changes. The results showed that there was a significant change in the heart rate (groups B and C), P-wave duration (group D), QT interval (groups B, C and D) and QTc (groups B, C and D) when compared to the control group. Histology also indicated that sections of the heart showed fatty infiltration of infl amed heart and areas of moderate inflammation of the atrium and ventricle. It could therefore be concluded from this study that though folklore indicated that corn silk (CS) is of high medicinal value, one must be careful in using this product as medicinal agent especially in patients with compromised heart conditions.

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“…Estimates of membrane potential in white blood cells vary from -45 to -86mV [19]. These negatively charged cells are presumably subject to electrostatic repulsion with respect to the negatively charged glycocalyx (electrical potential unknown) and the endothelial cell with trans membrane potential of -80mV, when polarized at extracellular potassium ion (K + ) concentration of 4mM [20]. This could explain, at least in part, the modulation of immobilization of leukocytes at the endothelial surface [21].…”

Section: Electrophysiological Aspectsmentioning

confidence: 99%

Development of the damaged glycocalyx hypothesis - A review

Drake-Holland¹,

Noble²

2018

Cardiovasc Disord Med

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We have reviewed the literature from 2008 up to 2018 that is relevant to our 2008 postulate that arterial glycocalyx dysfunction is the first step in the atherothombotic process. It would appear from this survey that the hypothesis is still a reasonable one. Vascular glycocalyx dysfunction has been shown to alter fluid exchange with tissue and is involved in oedema and iflammation formation, leading to revised equations for the Starling principle. Interactions between anticoagulant factors bound to the vascular glycocalyx have been postulated to protect vessels from intravascular thombosis. The glycocalyx, according to all authors that we have reviewd, is negatively charged, but we found no measurement of glycocalyx electrical potential. This negativity is suggested as a mechanism for repulsion of adhesion molecules. We suggest that future work should focus on the electrophysiology, e.g., endothelial cells are highly negatively charged, as are leukocytes and platelets. We postulate that electrostatic repulsion of like charges may play an important role in the protective function of the vascular glycocalyx, and its failure during dysfunction may contribute to the initiation of arterial disease.

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Membrane potential depolarization decreases the stiffness of vascular endothelial cells

Cited by 80 publications

References 66 publications

NaV1.5 sodium channels allosterically regulate the NHE-1 exchanger and promote breast cancer cell invadopodial activity

NaV1.5 sodium channels allosterically regulate the NHE-1 exchanger and promote breast cancer cell invadopodial activity

Cardiotoxicity Study of the Aqueous Extract of Corn Silk in Rats

Development of the damaged glycocalyx hypothesis - A review

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