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Updated: Oct 15, 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

Selective phosphotyrosine phosphatase inhibition and increased ceramide formation is associated with B-cell death by

G Dawson1, J Kilkus, G L Schieven

  • 1Department of Pediatrics, University of Chicago, IL 60637, USA. dawg@midway.uchicago.edu

FEBS Letters
|August 10, 2000
PubMed

Insights

Bis(maltolato)oxovanadium(IV) (BMOV) selectively triggers apoptosis in B-cells, not T-cells, by increasing ceramide levels. This suggests BMOV activates cell death pathways via sphingomyelinase in B-cells.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Immunology

Background:

  • Protein phosphotyrosine phosphatases (PTPs) regulate crucial cellular processes.
  • Dysregulation of PTPs is implicated in various diseases, including cancer.
  • Vanadium compounds, like Bis(maltolato)oxovanadium(IV) (BMOV), are known PTP inhibitors.

Purpose of the Study:

  • To investigate the selective effects of BMOV on apoptosis in different immune cell types.
  • To elucidate the molecular mechanisms underlying BMOV-induced apoptosis.
  • To explore the role of ceramide and sphingomyelinase in BMOV's action.

Main Methods:

  • Utilized TUNEL staining to quantify apoptosis in B-cell (Ramos) and T-cell (Jurkat) lines.
  • Analyzed protein tyrosine phosphorylation patterns in response to BMOV.
  • Measured ceramide and sphingomyelin levels in B-cells and T-cells treated with BMOV.

Main Results:

  • BMOV selectively induced apoptosis in Ramos B-cells but not in Jurkat T-cells.
  • Distinct patterns of protein tyrosine phosphorylation were observed between B-cells and T-cells upon BMOV treatment.
  • BMOV caused a twofold increase in ceramide levels and the ceramide/sphingomyelin ratio in B-cells, but not T-cells.

Conclusions:

  • BMOV-induced apoptosis in B-cells is mediated by increased ceramide levels, likely through sphingomyelinase activation.
  • Sustained tyrosine phosphorylation of specific proteins appears to trigger sphingomyelinase activation and the subsequent cell death pathway in B-cells.
  • BMOV exhibits selective cytotoxicity towards B-cells, highlighting its potential as a targeted therapeutic agent.

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