IL-5 Inhibits Apoptosis by Upregulation of c-myc Expression in Human Hematopoietic Cells

• Published in: Annals of the New York Academy of Sciences 2005-05, Vol.1042 (1), p.481-487
• Main Authors: JUAN, SHU-HUI, YEN, JEFFREY JONG-YOUNG, LEE, HORNG-MO, HUANG, HUEI-MEI
• Format: Article
• Language: English
• Subjects: anti-apoptosis; Apoptosis; Apoptosis - drug effects; Binding; Biotechnology; c-myc; Cell Line; Differentiation; Hematopoietic System - metabolism; Human; Humans; IL-5 receptor α subunit; interleukin 5; Interleukin-5 - pharmacology; Proto-Oncogene Proteins c-myc - genetics; Proto-Oncogene Proteins c-myc - metabolism; Receptors; Stimulation; Survival; Up-Regulation - genetics
• ISSN: 0077-8923; 1749-6632
• DOI: 10.1196/annals.1338.041

: 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.