Data for: Jiadifenolide induces expression of cellular communication network factor (CCN) genes, and CCN2 possesses neurotrophic activity in neuronal precursor cells derived from human induced pluripotent stem cells

Jiadifenolide induces expression of cellular communication network factor (CCN) genes, and CCN2 possesses neurotrophic activity in neuronal precursor cells derived from human induced pluripotent stem cells

Jiadifenolide has been reported to have neurotrophin-like activity in primary rat cortical neurons, and also possesses neurotrophic effects in neuronal precursor cells derived from human induced pluripotent stem cells (hiPSCs), as we have previously reported. However, the molecular mechanisms by which jiadifenolide exerts its neurotrophic effects in rat and human neurons are unknown. Thus, we aimed to investigate the molecular mechanisms and pathways by which jiadifenolide promotes neurotrophic effects. Here, we found that jiadifenolide activated cellular communication network factor (CCN) signaling pathways by up-regulating mRNA level expression of CCN genes in human neuronal cells. We also found that CCN2 (also known as connective tissue growth factor, CTGF) protein promotes neurotrophic effects through activation of the p44/42 mitogen-activated protein kinase (MAPK) signaling pathway. This is the first discovery which connects neurotrophic effects with CCN signaling.

己二酚内酯诱导细胞通讯网络因子（CCN）基因的表达，且CCN2蛋白在源自人诱导多能干细胞（hiPSCs）的神经前体细胞中展现出神经营养活性。己二酚内酯已被证实具有类似于神经生长因子的神经营养作用，作用于原代大鼠皮质神经元，并如我们先前所报道，对源自人诱导多能干细胞的神经前体细胞亦具有神经营养效应。然而，己二酚内酯在鼠类和人类神经元中发挥神经营养作用的分子机制尚不明确。因此，本研究旨在探究己二酚内酯促进神经营养作用的分子机制及途径。本研究发现，己二酚内酯通过上调人神经元细胞中CCN基因的mRNA水平表达，激活了细胞通讯网络因子（CCN）信号通路。此外，我们还发现CCN2蛋白（亦称为结缔组织生长因子，CTGF）通过激活p44/42丝裂原活化蛋白激酶（MAPK）信号通路来促进神经营养作用。这一发现首次将神经营养作用与CCN信号通路联系起来。