['In a previous study, we observed cell proliferation 3 days after spinal cord injury, and levels of interleukin-6 (IL-6) and epidermal growth factor (EGF) had significantly increased in the region of the injury.', 'The purpose of the new study described here was to evaluate the roles of IL-6 and EGF after traumatic damage to the spinal cord having isolated neural progenitor cells (NPC) from adult mice.', 'Evidence provided by the trypan blue dye exclusion assay, 5-bromodeoxyuridine immunoreactivity and Western blot analysis indicated that IL-6 and EGF induced proliferation of these spinal cord-derived NPCs via phosphorylation of Janus-activated kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) and mitogen-activated protein kinases (MAPK), respectively. Combined treatment with IL-6 and EGF accelerated proliferation of cells synergistically and phosphorylation of STAT3 and extracellular signal-regulated kinase 1/2 (Erk1/2). Furthermore, AG490 and AG1478, JAK2 inhibitor and EGFR inhibitor, respectively, prevented the IL-6- and EGF-induced proliferation of the cells. Interestingly, IL-6-activated MAPKs but EGF did not influence JAK2/STAT3 activation; AG490 specifically inhibited IL-6-induced Erk1/2 phosphorylation without affecting IL-6-induced phosphorylation of Raf and MEK1/2. These results indicate that IL-6 is directly involved in Erk1/2 activation via JAK2 and that Erk1/2 provides a signal bridge between the IL-6-induced JAK2/STAT3 pathway and EGF-induced MAPK pathway.'] Does interleukin-6 induce proliferation in adult spinal cord-derived neural progenitors via the JAK2/STAT3 pathway with EGF-induced MAPK phosphorylation?