Markus-Koch Annett, Schmitt Oliver, Seemann Susanne, Lukas Jan, Koczan Dirk, Ernst Mathias, Fuellen Georg, Wree Andreas, Rolfs Arndt, Luo Jiankai
Albrecht-Kossel-Institute for Neuroregeneration, Rostock University Medical Center, Gehlsheimer Straße 20, 18147 Rostock, Germany.
Institute of Anatomy, Rostock University Medical Center, Gertrudenstrsse 9, 18055 Rostock, Germany.
Cell Mol Biol Lett. 2017 Aug 18;22:16. doi: 10.1186/s11658-017-0045-1. eCollection 2017.
ADAM23 is widely expressed in the embryonic central nervous system and plays an important role in tissue formation.
In this study, we showed that ADAM23 contributes to cell survival and is involved in neuronal differentiation during the differentiation of human neural progenitor cells (hNPCs). Upregulation of ADAM23 in hNPCs was found to increase the number of neurons and the length of neurite, while its downregulation decreases them and triggers cell apoptosis. RNA microarray analysis revealed mechanistic insights into genes and pathways that may become involved in multiple cellular processes upon up- or downregulation of ADAM23.
Our results suggest that ADAM23 regulates neuronal differentiation by triggering specific signaling pathways during hNPC differentiation.
ADAM23在胚胎中枢神经系统中广泛表达,并在组织形成中发挥重要作用。
在本研究中,我们表明ADAM23有助于细胞存活,并参与人类神经祖细胞(hNPCs)分化过程中的神经元分化。发现hNPCs中ADAM23的上调会增加神经元数量和神经突长度,而其下调则会减少它们并引发细胞凋亡。RNA微阵列分析揭示了ADAM23上调或下调时可能参与多种细胞过程的基因和途径的机制见解。
我们的结果表明,ADAM23在hNPCs分化过程中通过触发特定信号通路来调节神经元分化。