Draxin regulates hippocampal neurogenesis in the postnatal dentate gyrus by inhibiting DCC-induced apoptosis.
Draxin regulates hippocampal neurogenesis in the postnatal dentate gyrus by inhibiting DCC-induced apoptosis.
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DOI：
10.1038/s41598-018-19346-6
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发表时间：
2018-01-16
影响因子：
4.6
通讯作者：
Tanaka H
中科院分区：
文献类型：
--
作者：
Tawarayama H;Yamada H;Amin R;Morita-Fujimura Y;Cooper HM;Shinmyo Y;Kawata M;Ikawa S;Tanaka H
海马齿状回（DG）的神经发生是由可扩散的分子控制的，这些分子调节神经发生过程，包括细胞增殖、分化和存活。为了阐明海马神经发生的机制，我们研究了Draxin的功能，最初被确定为神经化学排斥剂，在DG神经元存活的调节。Draxin在齿状颗粒细胞系的Tbr 2（+）晚期祖细胞和NeuroD 1（+）成神经细胞中表达，而其受体DCC（在结直肠癌中缺失）的表达主要在成神经细胞中检测到。我们的表型分析显示，Draxin缺乏导致神经源性区域中DCC表达的成神经细胞凋亡增强。此外，使用海马神经干/祖细胞（HNSPC）系的体外试验表明，draxin抑制分化中表达DCC的HNSPCs的凋亡。总而言之，我们假设Draxin作为DCC的依赖受体配体，在出生后DG神经发生中发挥着关键作用，以维持和促进成神经细胞的存活。
Hippocampal neurogenesis in the dentate gyrus (DG) is controlled by diffusible molecules that modulate neurogenic processes, including cell proliferation, differentiation and survival. To elucidate the mechanisms underlying hippocampal neurogenesis, we investigated the function of draxin, originally identified as a neural chemorepellent, in the regulation of neuronal survival in the DG. Draxin was expressed in Tbr2 (+) late progenitors and NeuroD1 (+) neuroblasts in the dentate granule cell lineage, whereas expression of its receptor DCC (deleted in colorectal cancer) was mainly detectable in neuroblasts. Our phenotypic analysis revealed that draxin deficiency led to enhanced apoptosis of DCC-expressing neuroblasts in the neurogenic areas. Furthermore, in vitro assays using a hippocampal neural stem/progenitor cell (HNSPC) line indicated that draxin inhibited apoptosis in differentiating HNSPCs, which express DCC. Taken together, we postulate that draxin plays a pivotal role in postnatal DG neurogenesis as a dependence receptor ligand for DCC to maintain and promote survival of neuroblasts.
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