The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis
J. Clin. Invest. Armin Schneider, et al. 115:2083 doi:10.1172/JCI23559 [Go to this article.]

Figure 7
G-CSF counteracts programmed cell death in rat cortical neurons (A–D) and human neuroblastoma cells (SHSY-5Y) (E) in vitro. (A) The G-CSF receptor is present on primary cortical neurons in culture as shown by immunocytochemistry. (B) G-CSF of both human (h) and mouse (m) origin counteracts camptothecin-induced programmed cell death in primary neurons as determined by caspase-3/7 activity. (C) Preincubation of primary neurons with an antibody against the G-CSF receptor abolishes the antiapoptotic activity of G-CSF (not significant). (D) The NO donor NOR3 [(±)E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide] (150 μM) induces apoptosis in primary neurons as evidenced by PARP and caspase-3 cleavage (immunoblots, first and second lanes), which is reduced by G-CSF treatment (third lane). (E) Also in the human neuroblastoma cell line SHSY-5Y, human or mouse G-CSF reduces caspase activation by the NO donor NOR3. Bar graphs show relative caspase activity levels after normalization to control values. Rel. units, relative units.