Ghrelin suppresses proliferation of fetal neural progenitor cells, and induces their differentiation into neurons.

ABSTRACT

Although considerable progress has been made in understanding how the temporal and regional control of neural progenitor cells (NPCs) dictates their fate, their key regulators during neural development are still unknown. Ghrelin, which is isolated from porcine stomach extract, is an endogenous ligand for the growth hormone secretagogue receptor (GHS-R). The widespread expression of ghrelin and GHS-R in the central nervous system during development suggests that ghrelin may be involved in developmental neural growth. However, its role in regulating fetal NPCs is still unclear. In this study, we investigated the effects of ghrelin on primary cultured NPCs derived from fetal mouse telencephalon. The expressions of both ghrelin and its receptor were observed in NPCs using RT-PCR, immunoblotting and immunocytostaining. Interestingly, the exposure of fetal NPCs to ghrelin at concentrations of 10(-7) and 10(-9)M suppressed their proliferation, and caused them to differentiate into neurons and to extend neurites. These results strongly suggest that ghrelin plays an autocrine modulatory role in fetal neural development.