ArticleAmerican journal of physiology. Renal physiology2014
Cytochalasin E alters the cytoskeleton and decreases ENaC activity in Xenopus 2F3 cells.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Activity and function of the endothelial sodium channel is regulated by the effector domain of MARCKS-like protein 1 in mouse aortic endothelial cells.American journal of physiology. Cell physiology · 2025Article
- Chemically induced phenotype plasticity in the unicellular zygnematophyte, Penium margaritaceum.Protoplasma · 2024Article
- Cytochalasans and Their Impact on Actin Filament Remodeling.Biomolecules · 2023Review
- Article
- The diverse functions of the DEG/ENaC family: linking genetic and physiological insights.The Journal of physiology · 2023Article
- The Pharmacological Inhibition of CaMKII Regulates Sodium Chloride Cotransporter Activity in mDCT15 Cells.Biology · 2021Article
- Mal protein stabilizes luminal membrane PLC-β3 and negatively regulates ENaC in mouse cortical collecting duct cells.American journal of physiology. Renal physiology · 2019Article
- Direct and indirect inhibition of the circadian clock protein Per1: effects on ENaC and blood pressure.American journal of physiology. Renal physiology · 2019Article
- Lipidomic and proteomic analysis of exosomes from mouse cortical collecting duct cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- ENaC activity is regulated by calpain-2 proteolysis of MARCKS proteins.American journal of physiology. Cell physiology · 2017Article
- Ankyrin G Expression Regulates Apical Delivery of the Epithelial Sodium Channel (ENaC).The Journal of biological chemistry · 2017Article
- Epithelial Sodium Channel-α Mediates the Protective Effect of the TNF-Derived TIP Peptide in Pneumolysin-Induced Endothelial Barrier Dysfunction.Frontiers in immunology · 2017Article
- The Lectin-like Domain of TNF Increases ENaC Open Probability through a Novel Site at the Interface between the Second Transmembrane and C-terminal Domains of the α-Subunit.The Journal of biological chemistry · 2016Article
- Article
- Calmodulin and CaMKII modulate ENaC activity by regulating the association of MARCKS and the cytoskeleton with the apical membrane.American journal of physiology. Renal physiology · 2015Article
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9 authors at 1 institution in 1 country.
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Abstract
Numerous reports have linked cytoskeleton-associated proteins with the regulation of epithelial Na(+) channel (ENaC) activity. The purpose of the present study was to determine the effect of actin cytoskeleton disruption by cytochalasin E on ENaC activity in Xenopus 2F3 cells. Here, we show that cytochalasin E treatment for 60 min can disrupt the integrity of the actin cytoskeleton in cultured Xenopus 2F3 cells. We show using single channel patch-clamp experiments and measurements of short-circuit current that ENaC activity, but not its density, is altered by cytochalasin E-induced disruption of the cytoskeleton. In nontreated cells, 8 of 33 patches (24%) had no measurable ENaC activity, whereas in cytochalasin E-treated cells, 17 of 32 patches (53%) had no activity. Analysis of those patches that did contain ENaC activity showed channel open probability significantly decreased from 0.081 ± 0.01 in nontreated cells to 0.043 ± 0.01 in cells treated with cytochalasin E. Transepithelial current from mpkCCD cells treated with cytochalasin E, cytochalasin D, or latrunculin B for 60 min was decreased compared with vehicle-treated cells. The subcellular expression of fodrin changed significantly, and several protein elements of the cytoskeleton decreased at least twofold after 60 min of cytochalasin E treatment. Cytochalasin E treatment disrupted the association between ENaC and myristoylated alanine-rich C-kinase substrate. The results presented here suggest disruption of the actin cytoskeleton by different compounds can attenuate ENaC activity through a mechanism involving changes in the subcellular expression of fodrin, several elements of the cytoskeleton, and destabilization of the ENaC-myristoylated alanine-rich C-kinase substrate complex.
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