ArticleApoptosis : an international journal on programmed cell death2010
Ouabain-induced perturbations in intracellular ionic homeostasis regulate death receptor-mediated apoptosis.
Article in Apoptosis : an international journal on programmed cell death, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Ouabain Protects Nephrogenesis in Rats Experiencing Intrauterine Growth Restriction and Partially Restores Renal Function in Adulthood.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Transient Receptor Potential Vanilloid 1 Expression Mediates Capsaicin-Induced Cell Death.Frontiers in physiology · 2018Article
- Na⁺Molecules (Basel, Switzerland) · 2017Review
- Much More than a Cardiotonic Steroid: Modulation of Inflammation by Ouabain.Frontiers in physiology · 2017Review
- Ouabain Enhances ADPKD Cell Apoptosis via the Intrinsic Pathway.Frontiers in physiology · 2016Article
- Analysis of proliferation and apoptotic induction by 20 steroid glycosides in 143B osteosarcoma cells in vitro.Cell proliferation · 2015Article
- Ion channels and transporters in the development of drug resistance in cancer cells.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- Translocation of mixed lineage kinase domain-like protein to plasma membrane leads to necrotic cell death.Cell research · 2014Article
- Rebuttal from Sergei N. Orlov, Michael M. Model and Ryszard Grygorczyk.The Journal of physiology · 2013Article
- CrossTalk proposal: Cell volume changes are an essential step in the cell death machinery.The Journal of physiology · 2013Article
- The death of ouabain-treated renal epithelial C11-MDCK cells is not mediated by swelling-induced plasma membrane rupture.The Journal of membrane biology · 2011Article
- Potassium ion fluxes in corneal epithelial cells exposed to UVB.Experimental eye research · 2011Article
- The Na+/H+ exchanger controls deoxycholic acid-induced apoptosis by a H+-activated, Na+-dependent ionic shift in esophageal cells.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Apoptosis is defined by specific morphological and biochemical characteristics including cell shrinkage (termed apoptotic volume decrease), a process that results from the regulation of ion channels and plasma membrane transporter activity. The Na(+)-K(+)-ATPase is the predominant pump that controls cell volume and plasma membrane potential in cells and alterations in its function have been suggested to be associated with apoptosis. We report here that the Na(+)-K(+)-ATPase inhibitor ouabain, potentiates apoptosis in the human lymphoma Jurkat cells exposed to Fas ligand (FasL) or tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) but not other apoptotic agents such as H(2)O(2), thapsigargin or UV-C implicating a role for the Na(+)-K(+)-ATPase in death receptor-induced apoptosis. Interestingly, ouabain also potentiated perturbations in cell Ca(2+) homeostasis only in conjunction with the apoptotic inducer FasL but not TRAIL. Ouabain did not affect alterations in the intracellular Ca(2+) levels in response to H(2)O(2), thapsigargin or UV-C. FasL-induced alterations in Ca(2+) were not abolished in Ca(2+)-free medium but incubation of cells with BAPTA-AM inhibited both Ca(2+) perturbations and the ouabain-induced potentiation of FasL-induced apoptosis. Our data suggest that the impairment of the Na(+)-K(+)-ATPase activity during apoptosis is linked to perturbations in cell Ca(2+) homeostasis that modulate apoptosis induced by the activation of Fas by FasL.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.