ArticleMolecular biology of the cell2004
Cardiac steroids induce changes in recycling of the plasma membrane in human NT2 cells.
Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 40 citations in OpenAlex.
- Bufalin-Induced Epithelial-to-Mesenchymal Transition in Kidney Epithelial Cells.Cell biology international · 2025Article
- Loss of the Na+/K+ cation pump CATP-1 suppresses nekl-associated molting defects.G3 (Bethesda, Md.) · 2024Article
- Markedly divergent effects of Ouabain on a Temozolomide-resistant (T98G) vs. a Temozolomide-sensitive (LN229) Glioblastoma cell line.Discover oncology · 2023Article
- Depth of the Steroid Core Location Determines the Mode of Na,K-ATPase Inhibition by Cardiotonic Steroids.International journal of molecular sciences · 2021Article
- Ouabain-Induced Cell Death and Survival. Role of α1-Na,K-ATPase-Mediated Signaling and [NaFrontiers in physiology · 2020Review
- Na⁺Molecules (Basel, Switzerland) · 2017Review
- Critical role of the α1-Na(+), K(+)-ATPase subunit in insensitivity of rodent cells to cytotoxic action of ouabain.Apoptosis : an international journal on programmed cell death · 2015Article
- 21-Benzylidene digoxin: a proapoptotic cardenolide of cancer cells that up-regulates Na,K-ATPase and epithelial tight junctions.PloS one · 2014Article
- Human breast tumor cells are more resistant to cardiac glycoside toxicity than non-tumorigenic breast cells.PloS one · 2013Article
- Formation of new high density glycogen-microtubule structures is induced by cardiac steroids.The Journal of biological chemistry · 2012Article
- Ouabain attenuates cardiotoxicity induced by other cardiac steroids.British journal of pharmacology · 2010Article
- [Na+]i/[K+]i -independent death of ouabain-treated renal epithelial cells is not mediated by Na+,K+ -ATPase internalization and de novo gene expression.Pflugers Archiv : European journal of physiology · 2008Article
- Cardenolide-induced lysosomal membrane permeabilization demonstrates therapeutic benefits in experimental human non-small cell lung cancers.Neoplasia (New York, N.Y.) · 2006Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac steroids (CSs) are specific inhibitors of Na+, K(+)-ATPase activity. Although the presence of CS-like compounds in animal tissues has been established, their physiological role is not evident. In the present study, treatment of human NT2 cells with physiological concentrations (nanomolar) of CSs caused the accumulation of large vesicles adjacent to the nucleus. Experiments using N-(3-triethylammonium propyl)-4-(dibutilamino)styryl-pyrodinum dibromide, transferrin, low-density lipoprotein, and selected anti-transferrin receptor and Rab protein antibodies revealed that CSs induced changes in endocytosis-dependent membrane traffic. Our data indicate that the CS-induced accumulation of cytoplasmic membrane components is a result of inhibited recycling within the late endocytic pathway. Furthermore, our results support the notion that the CS-induced changes in membrane traffic is mediated by the Na+, K(+)-ATPase. These phenomena were apparent in NT2 cells at nanomolar concentrations of CSs and were observed also in other human cell lines, pointing to the generality of this phenomenon. Based on these observations, we propose that the endogenous CS-like compounds are physiological regulators of recycling of endocytosed membrane proteins and cargo.
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