IL-5 inhibits apoptosis by upregulation of c-myc expression in human hematopoietic cells

Shu Hui Juan, Jeffrey Jong Young Yen, Horng Mo Lee, Huei Mei Huang

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Interleukin 5 (IL-5) inhibition of apoptosis is required throughout many hematopoietic lineages to regulate proliferation and differentiation. It is not clear how IL-5 mediates the intracellular molecular events regulating the anti-apoptotic effect. The cell lines TF-1 and JYTF-1 expressed different amounts of the IL-5 receptor α (IL-5Rα) subunit, which caused contrasting effects in response to IL-5. IL-5 supported the survival but not the anti-apoptotic activities of TF-1 cells, which have a low expression of IL-5Rα. In contrast, IL-5 supported both the survival and the anti-apoptotic activities of JYTF-1 cells, which overexpressed IL-5Rα compared to TF-1 cells. In this study, IL-5 stimulation increased Annexin V binding (indicative of apoptosis) in TF-1 cells and decreased apoptosis in JYTF-1 cells. The proto-oncogenes c-fos, fosB, and c-jun were not detected, whereas junB was induced by IL-5 stimulation in both types of cells. Most importantly, IL-5 significantly induced c-myc expression in JYTF-1 cells, but did not in TF-1 cells. These results are consistent with the possibility that IL-5 inhibits apoptosis in JYTF-1 cells via the upregulation of c-myc expression.

Original languageEnglish
Pages (from-to)481-487
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume1042
DOIs
Publication statusPublished - 2005

Fingerprint

Interleukin-5
Up-Regulation
Apoptosis
Interleukin-5 Receptors
fos Genes
Cells
Survival
Annexin A5
Cell Line

Keywords

  • Anti-apoptosis
  • c-myc
  • IL-5 receptor α subunit
  • Interleukin 5

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

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title = "IL-5 inhibits apoptosis by upregulation of c-myc expression in human hematopoietic cells",
abstract = "Interleukin 5 (IL-5) inhibition of apoptosis is required throughout many hematopoietic lineages to regulate proliferation and differentiation. It is not clear how IL-5 mediates the intracellular molecular events regulating the anti-apoptotic effect. The cell lines TF-1 and JYTF-1 expressed different amounts of the IL-5 receptor α (IL-5Rα) subunit, which caused contrasting effects in response to IL-5. IL-5 supported the survival but not the anti-apoptotic activities of TF-1 cells, which have a low expression of IL-5Rα. In contrast, IL-5 supported both the survival and the anti-apoptotic activities of JYTF-1 cells, which overexpressed IL-5Rα compared to TF-1 cells. In this study, IL-5 stimulation increased Annexin V binding (indicative of apoptosis) in TF-1 cells and decreased apoptosis in JYTF-1 cells. The proto-oncogenes c-fos, fosB, and c-jun were not detected, whereas junB was induced by IL-5 stimulation in both types of cells. Most importantly, IL-5 significantly induced c-myc expression in JYTF-1 cells, but did not in TF-1 cells. These results are consistent with the possibility that IL-5 inhibits apoptosis in JYTF-1 cells via the upregulation of c-myc expression.",
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author = "Juan, {Shu Hui} and Yen, {Jeffrey Jong Young} and Lee, {Horng Mo} and Huang, {Huei Mei}",
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AU - Juan, Shu Hui

AU - Yen, Jeffrey Jong Young

AU - Lee, Horng Mo

AU - Huang, Huei Mei

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AB - Interleukin 5 (IL-5) inhibition of apoptosis is required throughout many hematopoietic lineages to regulate proliferation and differentiation. It is not clear how IL-5 mediates the intracellular molecular events regulating the anti-apoptotic effect. The cell lines TF-1 and JYTF-1 expressed different amounts of the IL-5 receptor α (IL-5Rα) subunit, which caused contrasting effects in response to IL-5. IL-5 supported the survival but not the anti-apoptotic activities of TF-1 cells, which have a low expression of IL-5Rα. In contrast, IL-5 supported both the survival and the anti-apoptotic activities of JYTF-1 cells, which overexpressed IL-5Rα compared to TF-1 cells. In this study, IL-5 stimulation increased Annexin V binding (indicative of apoptosis) in TF-1 cells and decreased apoptosis in JYTF-1 cells. The proto-oncogenes c-fos, fosB, and c-jun were not detected, whereas junB was induced by IL-5 stimulation in both types of cells. Most importantly, IL-5 significantly induced c-myc expression in JYTF-1 cells, but did not in TF-1 cells. These results are consistent with the possibility that IL-5 inhibits apoptosis in JYTF-1 cells via the upregulation of c-myc expression.

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