The Children's Hospital, National Clinical Research Center for Child Health, Zhejiang University School of Medicine, Hangzhou 310052, China.
The Institute of Translational Medicine, School of Medicine, Zhejiang University, Hangzhou 310029, China.
Cells. 2022 Apr 9;11(8):1283. doi: 10.3390/cells11081283.
Nicotinamide adenine dinucleotide hydrate (NAD+) acts as the essential component of the tricarboxylic citric acid (TCA) cycle and has important functions in diverse biological processes. However, the roles of NAD+ in regulating adult neural stem/progenitor cells (aNSPCs) remain largely unknown. Here, we show that NAD+ exposure leads to the reduced proliferation and neuronal differentiation of aNSPCs and induces the apoptosis of aNSPCs. In addition, NAD+ exposure inhibits the morphological development of neurons. Mechanistically, RNA sequencing revealed that the transcriptome of aNSPCs is altered by NAD+ exposure. NAD+ exposure significantly decreases the expression of multiple genes related to ATP metabolism and the PI3k-Akt signaling pathway. Collectively, our findings provide some insights into the roles and mechanisms in which NAD+ regulates aNSPCs and neuronal development.
烟酰胺腺嘌呤二核苷酸水合物（NAD+）是三羧酸柠檬酸（TCA）循环的必需组成部分，在多种生物过程中具有重要功能。然而，NAD+在调节成体神经干细胞/祖细胞（aNSPCs）中的作用在很大程度上尚不清楚。在这里，我们表明 NAD+暴露导致 aNSPCs 的增殖和神经元分化减少，并诱导 aNSPCs 的细胞凋亡。此外，NAD+暴露抑制神经元的形态发育。在机制上，RNA 测序显示 NAD+暴露改变了 aNSPCs 的转录组。NAD+暴露显著降低了与 ATP 代谢和 PI3k-Akt 信号通路相关的多个基因的表达。总的来说，我们的研究结果为 NAD+调节 aNSPCs 和神经元发育的作用和机制提供了一些见解。
