Dual function of IL-33 on proliferation of NIH-3T3 cells

• Published in: Cytokine (Philadelphia, Pa.) Vol. 72; no. 1; pp. 105 - 108
• Main Authors: Tominaga, Shin-ichi, Tago, Kenji, Tsuda, Hidetoshi, Komine, Mayumi
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.03.2015
• Subjects: Animals; Apoptosis - drug effects; Cell growth; Cell Proliferation - drug effects; Fibroblast; IL-33; Interleukin-33; Interleukins - pharmacology; Interleukins - physiology; Ligands; Mice; NIH 3T3 Cells; Recombinant Proteins - pharmacology; ST2 gene; DMEM; FITC; Cell growth; FBS; ST2 gene; S.D; IL-1R; NIH-3T3 cells; IL-33; Fibroblast
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1016/j.cyto.2014.12.004

•The paper reports a novel dual effect of IL-33 on cell proliferation.•IL-33 treatment suppresses initiation of cell growth of NIH-3T3 cells.•The effect is not caused by apoptotic cell death. The interleukin-33 (IL-33)-ST2L signaling pathway has been shown to play important roles in the field of immunology, especially as a trigger for allergic reactions such as bronchial asthma. However, coming back to the original finding that the ST2 gene is induced during initiation of the cell cycle of fibroblastic cell lines, the possible functions of the ST2 gene products and their specific ligand, IL-33, in the field of cell growth regulation are still interesting problems to be solved. In this study, we used NIH-3T3 mouse cell line and added IL-33 before and after cell proliferation assay, which revealed the dual function of IL-33. When IL-33 was added to the confluent cells before the start of cell proliferation, it suppressed the cell growth concentration-dependently. On the other hand, if IL-33 was added after the start of cell proliferation, it enhanced the cell growth. The negative effect of IL-33 on cell proliferation is a novel finding and would provide an important clue to the roles of IL-33 and ST2/ST2L in growth regulation.