Role of c-jun in the inhibition of erythropoietin receptor-mediated apoptosis

Biochem Biophys Res Commun. 1996 May 6;222(1):1-6. doi: 10.1006/bbrc.1996.0688.

Abstract

Human bone marrow cells express both a truncated and full-length form of the erythropoietin receptor (EpoR-T and EpoR-F, respectively). Transfection experiments using the murine interleukin (IL)-3-dependent cell line, Ba/F3, revealed that the cells coexpressing EpoR-F and EpoR-T (Ba/F3-FT) were more likely to undergo programmed cell death (apoptosis) than cells expressing EpoR-F (Ba/F3-FF), even in the presence of erythropoietin (Epo). When Ba/F3-FF cells were stimulated with Epo or IL-3, rapid induction of c-myc, c-fos, c-jun and junB genes was observed. A similar effect was also seen in IL-3 stimulated Ba/F3-Ft cells. However, in Ba/F3-FT cells expression of the c-jun gene was not induced by Epo stimulation. Administration of Epo could prevent apoptosis induced by IL-3 deprivation in Ba/F3-FT cells expressing ectopic c-Jun protein. These results indicate that induction of c-Jun through the Epo signaling pathway has an important role in the inhibition of apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cells, Cultured
  • Erythropoietin / physiology*
  • Gene Expression
  • Genes, fos
  • Genes, jun
  • Humans
  • Mice
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-jun / physiology*
  • RNA, Messenger / genetics
  • Receptors, Erythropoietin / physiology*
  • Signal Transduction

Substances

  • Proto-Oncogene Proteins c-fos
  • Proto-Oncogene Proteins c-jun
  • RNA, Messenger
  • Receptors, Erythropoietin
  • Erythropoietin