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首页> 外文期刊>Journal of Cellular Physiology >mSEL‐1L deficiency affects vasculogenesis and neural stem cell lineage commitment
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mSEL‐1L deficiency affects vasculogenesis and neural stem cell lineage commitment

机译：毫秒1 l不足影响血管生成和神经干细胞谱系的承诺

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摘要

mSEL‐1L is a highly conserved ER‐resident type I protein, involved in the degradation of misfolded peptides through the ubiquitin–proteasome system (UPS), a pathway known to control the plasticity of the vascular smooth muscle cells (VSMC) phenotype and survival. In this article, we demonstrate that mSEL‐1L deficiency interferes with the murine embryonic vascular network, showing particular irregularities in the intracranic and intersomitic neurovascular units and in the cerebral capillary microcirculation. During murine embryogenesis, mSEL‐1L is expressed in cerebral areas known to harbor progenitor neural cells, while in the adult brain the protein is specifically restricted to the stem cell niches, co‐localizing with Sox2 and Nestin. Null mice are characterized by important defects in the development of telenchephalic regions, revealing conspicuous aberration in neural stem cell lineage commitment. Moreover, mSEL‐1L depletion in vitro and in vivo appears to affect the harmonic differentiation of the NSCs, by negatively influencing the corticogenesis processes. Overall, the data presented suggests that the drastic phenotypic characteristics exhibited in mSEL‐1L null mice can, in part, be explained by the negative influence it plays on Notch1 signaling pathway.
机译：毫秒1 l是一个高度保守的ER应承担的居民I型错误折叠的蛋白质,参与降解肽通过ubiquitin-proteasome系统(UPS)通路控制塑性血管平滑肌细胞(VSMC)表型和生存。证明毫秒1 l缺陷影响与小鼠胚胎血管网络,显示特定的违规行为intracranic和intersomitic神经与血管的单位和脑毛细血管微循环。在小鼠胚胎发生,毫秒1 l表示在大脑区域港口祖神经细胞,而在成人大脑蛋白质是专门限制阀杆细胞利基市场,公司本地化与Sox2和巢蛋白。零老鼠的特点是重要的缺陷telenchephalic发展的地区,揭示在神经干细胞明显的畸变细胞谱系的承诺。损耗在体外和体内似乎影响nsc的谐波分化,通过负面影响corticogenesis流程。激烈的表型特征在毫秒高1 l零老鼠可以在部分用它发挥的负面影响来解释Notch1信号通路。

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