Small molecule inhibitor DDQ-treated hippocampal neuronal cells show improved neurite outgrowth and synaptic branching.

IF 5.9 2区 医学 Q2 CELL BIOLOGY Neural Regeneration Research Pub Date : 2025-09-01 Epub Date: 2024-06-19 DOI:10.4103/NRR.NRR-D-24-00157
Jangampalli Adi Pradeepkiran, Priyanka Rawat, Arubala P Reddy, Erika Orlov, P Hemachandra Reddy
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Abstract

JOURNAL/nrgr/04.03/01300535-202509000-00024/figure1/v/2024-11-05T132919Z/r/image-tiff The process of neurite outgrowth and branching is a crucial aspect of neuronal development and regeneration. Axons and dendrites, sometimes referred to as neurites, are extensions of a neuron's cellular body that are used to start networks. Here we explored the effects of diethyl (3,4-dihydroxyphenethylamino)(quinolin-4-yl) methylphosphonate (DDQ) on neurite developmental features in HT22 neuronal cells. In this work, we examined the protective effects of DDQ on neuronal processes and synaptic outgrowth in differentiated HT22 cells expressing mutant Tau (mTau) cDNA. To investigate DDQ characteristics, cell viability, biochemical, molecular, western blotting, and immunocytochemistry were used. Neurite outgrowth is evaluated through the segmentation and measurement of neural processes. These neural processes can be seen and measured with a fluorescence microscope by manually tracing and measuring the length of the neurite growth. These neuronal processes can be observed and quantified with a fluorescent microscope by manually tracing and measuring the length of the neuronal HT22. DDQ-treated mTau-HT22 cells (HT22 cells transfected with cDNA mutant Tau) were seen to display increased levels of synaptophysin, MAP-2, and β-tubulin. Additionally, we confirmed and noted reduced levels of both total and p-Tau, as well as elevated levels of microtubule-associated protein 2, β-tubulin, synaptophysin, vesicular acetylcholine transporter, and the mitochondrial biogenesis protein-peroxisome proliferator-activated receptor-gamma coactivator-1α. In mTau-expressed HT22 neurons, we observed DDQ enhanced the neurite characteristics and improved neurite development through increased synaptic outgrowth. Our findings conclude that mTau-HT22 (Alzheimer's disease) cells treated with DDQ have functional neurite developmental characteristics. The key finding is that, in mTau-HT22 cells, DDQ preserves neuronal structure and may even enhance nerve development function with mTau inhibition.

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小分子抑制剂 DDQ 处理的海马神经元细胞显示神经元突起生长和突触分支得到改善。
摘要:神经元的生长和分支过程是神经元发育和再生的一个重要方面。轴突和树突有时被称为神经元,是神经元细胞体的延伸,用于启动网络。在这里,我们探讨了(3,4-二羟基苯乙胺)(喹啉-4-基)甲基膦酸二乙酯(DDQ)对 HT22 神经元细胞神经元发育特征的影响。在这项工作中,我们研究了 DDQ 对表达突变型 Tau(mTau)cDNA 的分化 HT22 细胞的神经元过程和突触生长的保护作用。为了研究 DDQ 的特性,我们使用了细胞活力、生化、分子、Western 印迹和免疫细胞化学等方法。神经元生长是通过神经过程的分割和测量来评估的。使用荧光显微镜可通过手动追踪和测量神经元生长的长度来观察和测量这些神经过程。通过手动追踪和测量神经元 HT22 的长度,可以用荧光显微镜观察和量化这些神经元过程。经 DDQ 处理的 mTau-HT22 细胞(转染了 cDNA 突变体 Tau 的 HT22 细胞)显示突触素、MAP-2 和 β-tubulin 水平升高。此外,我们还证实并注意到总 Tau 和 p-Tau 水平降低,微管相关蛋白 2、β-tubulin、突触素、囊泡乙酰胆碱转运体和线粒体生物生成蛋白-过氧化物酶体增殖激活受体-gamma 辅激活剂-1α 水平升高。在表达 mTau 的 HT22 神经元中,我们观察到 DDQ 通过增加突触生长增强了神经元特征并改善了神经元发育。我们的研究结果表明,经 DDQ 处理的 mTau-HT22(阿尔茨海默病)细胞具有功能性神经元发育特征。关键的发现是,在 mTau-HT22 细胞中,DDQ 可保护神经元结构,甚至可能通过抑制 mTau 增强神经发育功能。
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来源期刊
Neural Regeneration Research
Neural Regeneration Research CELL BIOLOGY-NEUROSCIENCES
CiteScore
8.00
自引率
9.80%
发文量
515
审稿时长
1.0 months
期刊介绍: Neural Regeneration Research (NRR) is the Open Access journal specializing in neural regeneration and indexed by SCI-E and PubMed. The journal is committed to publishing articles on basic pathobiology of injury, repair and protection to the nervous system, while considering preclinical and clinical trials targeted at improving traumatically injuried patients and patients with neurodegenerative diseases.
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