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<br> Conclusion
Acknowledgments This work was supported by Progetto PON - “Ricerca e Competitività 2007–2013” - PON01_01802: “Sviluppo di molecole capaci di modulare vie metaboliche intracellulari redox-sensibili per la prevenzione e la cura di patologie infettive, tumorali, neurodegenerative e loro delivery mediante piattaforme nano tecnologiche” and PON01_02512: “Ricerca e sviluppo di bioregolatori attivi sui meccanismi epigenetici dei processi infiammatori nelle malattie croniche e degenerative.” The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.
Introduction Neural stem cells (NSCs) are defined by their ability to proliferate, self-renew and retain the potential to differentiate into neuronal and glial lineages [1–4]. They are responsible for early nervous system development and postnatal nervous tissue regeneration and repair [5–7]. Under normal conditions, neurogenesis in the adult mammalian CMX001 is restricted to two discrete germinal centers: the subgranular layer of the hippocampal dentate gyrus and the subventricular zones of the lateral ventricles [3,8,9]. Studies on NSCs provide a unique model system to understand basic mechanisms of neural differentiation, but also lead to improved strategies for neural tissue repair and cell-based replacement therapies in the nervous system and have the potential to ameliorate parkinson\'s disease, huntington\'s disease, stroke, and traumatic brain injury leading to partial functional recovery [10,11]. Although studies using stem cells provide hope, it is necessary to understand how to direct and control differentiation of specific target phenotypes required for replacement and repair in each disease, as well as to improve survival and differentiation levels of stem cells after transplantation [12,13]. Recently, several techniques have been adopted to regulate the differentiation, cell cycling or apoptosis of stem cells by over-expressing antioxidant genes such as ADC which can synthesize agmatine [14–16]. Despite several technical and safety problems, scientists have started to translate their basic scientific findings into therapies for untreatable diseases [17]. A complete understanding of neural stem cells requires the identification of molecules that determine the self-renewal and multi-potent characteristics of these cells. Several signaling pathways such as leukemia inhibitory factor (LIF), Wnt protein and bone morphogenetic proteins (BMPs), CAMs and integrins have been demonstrated to play a role in stem cell fate determination of growth and development [18–20]. However, molecular mechanisms underlying regulation of stem cell fate by these extracellular factors remain unknown. BMPs are members of the Transforming Growth Factor-Beta (TGF-β) family that play various, sometimes distinct roles throughout the development of the nervous system, often in a context and stage-dependent manner [21]. In early embryogenesis, BMPs inhibit neuro-ectoderm formation [22,23] whereas in late embryogenesis, BMPs promote the differentiation of both neuronal cells and astroglial cells [24–26]. BMPs execute their functions by binding to and activating BMP receptors I and II [27]. The BMP-Smad1/5/8 pathway is a major pathways controlling neurogenesis [28,29]. BMP receptor I phosphorylates Smad1/5/8 at the C-terminal SXS motif. Smad1/5/8 then associate with Smad4, move into the nucleus, and turn on BMP-target genes to initiate neurogenesis. BMP-regulated gene expression is controlled without dependence of cell-type through direct Smad binding and in a cell-type-specific manner via interaction with tissue-specific transcription factors. These Smad-dependent transcriptional targets coupled to cross-talk between the BMP and other signaling pathways likely mediate transcriptional programs associated with cell fate choices [29]. However, little is known about the BMP target genes except inhibitor of DNA binding/differentiation-1 (Id-1) that controls neurogenesis. BMP target gene, Id-1appears to mediate the inhibitory effects of BMPs on neuronal differentiation at least in mouse embryonic stem cells (ESC) [19]. Id-1 binds to pro-neuronal transcription factors such as Mammalian achaete-schute Homolog 1 (Mash1) to inhibit their function. Wnt signaling has long been implicated in neural crest induction [30], and in differentiation of melanocytes from cultured NSCs isolated from mouse neural tube [31]. Neural crest stem cells (NCSCs) lacking the Wnt signaling component,β-catenin, fail to generate sensory neurons [32]. While embryos expressing a constitutively active form of β-catenin in NCSCs develop sensory neurons at the expense of virtually all other neural crest derivatives [33].