DiSCAFF, University of Piemonte Orientale A. Avogadro, Novara, Italy.
Mol Cell Neurosci. 2010 Oct;45(2):139-50. doi: 10.1016/j.mcn.2010.06.005. Epub 2010 Jun 17.
The Receptor for Advanced Glycation End-products (RAGE) is a member of the immunoglobulin superfamily of cell surface receptors which interacts with a wide range of ligands, such as High-Mobility Group Box-1 (HMGB-1), S100B, advanced glycation end-products (AGEs). Here we provided evidence for the restricted expression of RAGE in the undifferentiated neural stem/progenitor cells of mouse adult SubVentricular Zone (SVZ) neurogenic region and adult SVZ-derived neurospheres. Additionally, RAGE ligands stimulated both proliferation and neuronal differentiation of SVZ-derived neural progenitor cells (NPC) in vitro. NF-kappaB nuclear translocation occurred upon RAGE activation in SVZ-derived neurospheres and its blockade (by SN-50) or its absence (in p50(-/-) derived NPC) resulted in the inhibition of the ligand-mediated effects on neuronal differentiation. These novel findings delineate an interesting scenario where the RAGE-NF-kappaB axis may contribute to regulate adult neural stem/progenitor cell function in physiological and possibly pathological conditions where this axis is upregulated.
晚期糖基化终产物受体（RAGE）是免疫球蛋白超家族细胞表面受体的成员，可与多种配体相互作用，如高迁移率族蛋白 B1（HMGB-1）、S100B、晚期糖基化终产物（AGE）。在这里，我们提供了证据表明 RAGE 在成年小鼠侧脑室下区（SVZ）神经发生区未分化的神经干细胞/祖细胞和成年 SVZ 来源的神经球中受到限制表达。此外，RAGE 配体在体外刺激 SVZ 来源的神经祖细胞（NPC）的增殖和神经元分化。NF-κB 核易位发生在 SVZ 来源的神经球中 RAGE 激活时，其阻断（通过 SN-50）或缺失（在 p50（-/-）衍生的 NPC 中）导致配体介导的对神经元分化的作用受到抑制。这些新发现描绘了一个有趣的情景，即 RAGE-NF-κB 轴可能有助于调节生理和可能病理条件下成年神经干细胞/祖细胞的功能，在这些条件下，该轴被上调。
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