Nicotine inhibits bFGF-induced neurite outgrowth through suppression of NO synthesis in H19-7 cells

Abstract

NO(Nitric oxide) has been known as a biological signaling molecule that can function either as a physiologically beneficial agent which is involved in essential functions such as differentiation or neurotransmission, or as a pathological agent, and NO is formed by endothelial (e), neuronal (n) and inducible (i) nitric oxide synthase (NOS). Although many biological effects of nicotine have been identified, the inhibitory effect of nicotine on NO-induced neurite outgrowth still remains undefined. In this study, we tried to elucidate how nicotine inhibits the basic fibroblast growth factor (bFGF)-induced neuronal differentiation of H19-7 cells and attempted to determine the role of iNOS/nNOS in this process. bFGF treatment resulted in increased NO synthesis. When we treated cell with nicotine, bFGF-induced NO synthesis and iNOS/nNOS expression were decreased. Treatment of bFGF also increased expression of brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and Neuro-D. Interestingly, nicotine treatment suppressed the expressions of BDNF, NT3 and Neuro-D, respectively , suggesting that nicotine might inhibits bFGF-induced neurite outgrowth in H19-7 cells. Taken together, NO is important in bFGF-induced neuronal differentiated H19-7 cells and nicotine inhibits bFGF-induced neuronal differentiation with NO formation.