Division of Oral Physiology, Tohoku University Graduate School of Dentistry, Sendai 980-8575, Japan.
Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer, Tohoku University, Sendai 980-8575, Japan.
Int J Mol Sci. 2020 Nov 7;21(21):8356. doi: 10.3390/ijms21218356.
Neuritogenesis is the process underling nervous system regeneration; however, optimal extracellular signals that can promote neuronal regenerative activities require further investigation. Previously, we developed a novel method for inducing neuronal differentiation in rat PC12 cells using temperature-controlled repeated thermal stimulation (TRTS) with a heating plate. Based on neurogenic sensitivity to TRTS, PC12 cells were classified as either hyper- or hyposensitive. In this study, we aimed to investigate the mechanism of hyposensitivity by establishing two PC12-derived subclones according to TRTS sensitivity during differentiation: PC12-P1F1, a hypersensitive subclone, and PC12-P1D10, a hyposensitive subclone. To characterize these subclones, cell size and neuritogenesis were evaluated in subclones treated with nerve growth factor (NGF), bone morphogenetic protein (BMP), or various TRTS. No significant differences in cell size were observed among the parental cells and subclones. BMP4- or TRTS-induced neuritogenesis was increased in PC12-P1F1 cells compared to that in the parental cells, while no neuritogenesis was observed in PC12-P1D10 cells. In contrast, NGF-induced neuritogenesis was observed in all three cell lines. Furthermore, a BMP inhibitor, LDN-193189, considerably inhibited TRTS-induced neuritogenesis. These results suggest that the BMP pathway might be required for TRTS-induced neuritogenesis, demonstrating the useful aspects of these novel subclones for TRTS research.
神经发生是神经系统再生的过程;然而,能够促进神经元再生活动的最佳细胞外信号仍需要进一步研究。此前,我们开发了一种使用加热板控制的温度循环热刺激(TRTS)诱导大鼠 PC12 细胞神经元分化的新方法。基于对 TRTS 的神经发生敏感性,将 PC12 细胞分为超敏或低敏。在这项研究中,我们旨在通过根据分化过程中对 TRTS 的敏感性建立两个 PC12 衍生的亚克隆来研究低敏性的机制:PC12-P1F1 是一个超敏亚克隆,PC12-P1D10 是一个低敏亚克隆。为了对这些亚克隆进行特征分析,在神经生长因子(NGF)、骨形态发生蛋白(BMP)或各种 TRTS 处理的亚克隆中评估细胞大小和神经突生成。亲本细胞和亚克隆之间的细胞大小没有明显差异。与亲本细胞相比,BMP4 或 TRTS 诱导的神经突生成在 PC12-P1F1 细胞中增加,而在 PC12-P1D10 细胞中未观察到神经突生成。相反,所有三种细胞系均观察到 NGF 诱导的神经突生成。此外,BMP 抑制剂 LDN-193189 显著抑制了 TRTS 诱导的神经突生成。这些结果表明,BMP 途径可能是 TRTS 诱导的神经突生成所必需的,这表明这些新型亚克隆在 TRTS 研究方面具有有用的方面。