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Related Experiment Video

Updated: May 28, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Endogenous ouabain regulates cell viability.

Moran Dvela1, Haim Rosen, Hagit Cohen Ben-Ami

  • 1Department of Medical Neurobiology, Institute for Medical Research Israel-Canada, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

American Journal of Physiology. Cell Physiology
|October 28, 2011
PubMed
Summary
This summary is machine-generated.

Endogenous ouabain (EO) regulates cell viability. Lowering EO reduced cell viability, while adding ouabain increased it, activating ERK1/2 signaling in neuronal cells.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Physiology

Background:

  • Endogenous cardiac steroid-like compounds, particularly endogenous ouabain (EO), circulate in humans and may bind to the Na(+)-K(+)-ATPase.
  • Previous studies indicate these steroids promote cell growth in cultures, but their role in cell viability and proliferation remains unexplored.

Purpose of the Study:

  • To investigate the role of endogenous ouabain (EO) in regulating cell viability and proliferation.
  • To explore the involvement of ERK1/2 signaling in EO-mediated cellular effects.

Main Methods:

  • Quantified EO in mammalian sera and cerebrospinal fluid.
  • Used anti-ouabain antibodies to reduce endogenous EO levels in cultured cell lines (NT2, PC12, COS-7).
  • Administered ouabain and bufalin, and an ERK1/2 inhibitor (U0126) to assess effects on cell viability, proliferation, and ERK1/2 activation.

Main Results:

  • Reduced serum EO levels decreased viability in NT2 cells, but not PC12 or COS-7 cells.
  • Low concentrations of ouabain, but not bufalin, enhanced NT2 and PC12 cell viability and proliferation.
  • Ouabain and bufalin activated ERK1/2 in NT2 cells; this activation was necessary for ouabain's effect on viability.
  • Anti-ouabain antibodies reduced serum-stimulated ERK1/2 activity in NT2 cells.

Conclusions:

  • Endogenous ouabain (EO) plays a significant role in regulating cell viability.
  • Activation of the ERK1/2 signaling pathway is essential, though not solely sufficient, for EO to induce cell viability.