Nitric Oxide Is an Essential Mediator for Neuronal Differentiation of Rat Primary Cortical Neuron Cells

Abstract

Nitric oxide (NO) regulates proliferation, differentiation and survival of neurons. Although NO is reported to involve in NGF-induced differentiation of PC12 cells, the role of NO has not been characterized in primary neuron cells. Therefore, we investigated the role of NO in neuronal differentiation of primary cortical neuron cells. Primary cortical neuron cells were prepared from rat embryos of embryonic day 18 and treated with NMMA (NOS inhibitor) or PTIO (NO scavenger). Neurite outgrowth of neuron cells was counted and the mRNA levels of p21, p27, c-jun and c-myc were measured by RT-PCR. Neurite outgrowth of primary cortical neuron cells was inhibited a little by NOS inhibitor and completely by NO scavenger. The mRNA levels of p21 and p27, differentiation-induced growth arrest genes were increased during differentiation, but they were decreased by NOS inhibitor or NO scavenger. On the other hand, the level of c-jun mRNA was not changed and the level of c-myc mRNA was increased during differentiation differently from previously reported. The levels of these mRNA were reversed in NOS inhibitor- or NO scavenger-treated cells. The level of nNOS protein was not changed but NOS activity was inhibited largely by NOS inhibitor or NO scavenger. These results suggest that NO is an essential mediator for neuronal differentiation of primary cortical neuron cells.

hESC Differentiation toward an Autonomic Neuronal Cell Fate Depends on Distinct Cues from the Co-Patterning Vasculature

“…We were able to discern the role that developing BVs play in NC differentiation. We show that EC-derived NO provides a molecular cue facilitating NC differentiation, consistent with its recognized role in differentiation ( Cheng et al., 2003; Reif et al., 2004; Chen et al., 2005; Luo et al., 2010; Oh et al., 2010; Carreira et al., 2012 ). Specification of NC is then further refined by direct contact with VSMCs via a homotypic T-cad interaction that drives differentiation toward an autonomic neuronal fate.…”

“…One candidate that we examined was NO because it is a key regulator of the neurovascular unit. Furthermore, NO can promote neurogenesis ( Chen et al., 2005; Reif et al., 2004; Carreira et al., 2012; Luo et al., 2010 ) and neuronal differentiation ( Cheng et al., 2003; Oh et al., 2010 ). In our transwell model, ECs, which express endothelial NO synthase (eNOS), were treated with the NOS inhibitor L-NMMA, while VSMCs and NCs were plated together in the top chamber.…”

Can proline‐rich polypeptide complex mimic the effect of nerve growth factor?

“…The effect of PRP/NP on activation of nNOS and NO release indicates that both peptides are able to modify nNOS function. Similar modifying functions were also observed by Oh et al [41].…”

Biological effects and mechanisms of shortwave radiation: a review

“…The indirect functions depend on the activation of downstream target enzymes adenylyl cyclase (AC) and soluble guanylyl cyclase (sGC); then, activated AC and sGC catalyze the synthesis of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), respectively, regulating multiple biological processes (i.e., inflammation, cell differentiation, apoptosis, blood flow, tissue repair, etc.) by CaM/nNOS/cAMP signaling and CaM/NO/cGMP signaling [ 41 , 46 , 47 ].…”