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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

Microarray analysis uncovers the induction of the proapoptotic BH3-only protein Bim in multiple models of

Zhengqi Wang1, Michael H Malone, Huiling He

  • 1Departments of Medicine and Pharmacology, Comprehensive Cancer Center, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, Ohio 44106, USA.

The Journal of Biological Chemistry
|April 5, 2003
PubMed

Insights

Glucocorticoids induce apoptosis by increasing the expression of Bim, a key protein that triggers programmed cell death. This finding reveals a novel mechanism in lymphoid cell death.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Glucocorticoid-induced apoptosis is a clinically relevant process.
  • Transcriptional mechanisms underlying this cell death pathway remain largely unknown.

Purpose of the Study:

  • To identify gene expression changes during dexamethasone-induced apoptosis.
  • To elucidate the role of specific genes in glucocorticoid-mediated lymphoid cell death.

Main Methods:

  • Oligonucleotide microarrays were used to analyze gene expression patterns.
  • Dexamethasone treatment was applied to murine lymphoma cell lines (S49.A2, WEHI7.2).
  • Gene induction was confirmed by immunoblotting in various cell types.

Main Results:

  • Dexamethasone induced diverse gene expression changes over 24 hours.
  • Previously known changes in c-Myc and NF-kappaB signaling were observed.
  • Unexpectedly, glucocorticoids significantly increased the expression of Bim, a pro-apoptotic protein.

Conclusions:

  • Dexamethasone induces apoptosis in lymphoid cells partly through the upregulation of Bim.
  • Bim induction is a novel mechanism contributing to glucocorticoid-mediated cell death.
  • This provides new insights into the transcriptional regulation of apoptosis.

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