Abstract
Interleukin 9 (IL‐9) stimulates the proliferation of various hematopoietic cell types. To elucidate the molecular mechanisms underlying the cell proliferation action, immediate‐early gene expression elicited by IL‐9 in a human factor‐dependent cell line, MO7e, was studied. IL‐9 stimulation resulted in a rapid and transient elevation of primary response genes including junB and c‐myc. The differential effects of protein kinase inhibitors, herbimycin A, genistein, and H‐7 on the steady‐state mRNA level and the transcription rate of junB and c‐myc genes triggered by IL‐9 were also investigated. Herbimycin A, but not genistein, specifically inhibited the expression of junB steady‐state mRNA and the in vitro transcription of the junB gene. IL‐9‐enhanced c‐myc gene expression was completely inhibited by both herbimycin A and genistein at the level of transcriptional initiation. H‐7 failed to inhibit c‐myc, but partially abolished junB mRNA induction. The role of protein kinase C in IL‐9‐mediated junB induction was also examined. The different responses of junB and c‐myc messages to protein kinase inhibitors suggested that more than one pathway may be involved in IL‐9‐mediated signal transduction which leads to the expression of junB and c‐myc genes. © 1995 Wiley‐Liss, Inc.