Lipid profile dataset of optogenetics induced optic nerve regeneration
Lipid profile dataset of optogenetics induced optic nerve regeneration
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DOI：
10.1016/j.dib.2020.106001
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发表时间：
2020-08-01
期刊：
影响因子：
1.2
通讯作者：
Bhattacharya, Sanjoy K.
中科院分区：
文献类型：
--
作者：
Arcuri, Jennifer;Liu, Yuan;Bhattacharya, Sanjoy K.
视神经通过视网膜神经节细胞（RGCs）的轴突将视觉信息从视网膜传递到大脑。在成年哺乳动物中，视神经损伤和进行性退行性疾病导致RGCs的不可逆丧失，导致视力丧失和失明。利用rgc特异性的thy-1启动子表达和刺激rgc中的通道视紫红质（Chr2），光遗传学模型已被证明在操纵rgc生长方面是有用的。我们使用转基因Chr2小鼠（Thy1-ChR2-EYFP）作为再生模型，研究了创伤性视神经压迫、光刺激和RGC轴突生长后的脂质变化。将Thy1-ChR2-EYFP小鼠和对照（C57BL/6）小鼠分为4组：1)无挤压和无刺激组，2)无挤压加刺激组，3)挤压加无刺激组，4)挤压加刺激组。安乐死后采集视神经进行脂质组学分析。脂质提取采用Bligh and Dyer法，质谱分析采用Q-Exactive Orbitrap液相色谱-质谱联用仪（LC MS-MS）。使用LipidSearch 4.1.3对原始扫描进行分析，使用Metaboanalyst 4.0进行统计分析。(C) 2020作者。Elsevier Inc.出版。
The optic nerve transfers visual information from the retina to the brain through the axons of retinal ganglion cells (RGCs). In adult mammals, optic nerve injuries and pro-gressive degenerative diseases lead to the irreversible loss of RGCs, resulting in vision loss and blindness. Optogenetic models have proved useful in manipulating the growth of RGCs through expression and stimulation of channel-rhodopsins (Chr2) in RGCs using the RGC-specific thy-1 promoter. Using transgenic Chr2 mouse (Thy1-ChR2-EYFP) as a model of regeneration, we profile the lipid changes which occur after traumatic optic nerve crush, light stimulation and forced RGC axonal growth. Thy1-ChR2-EYFP and control (C57BL/6) mice were divided in four groups each - 1) no crush and no stimulation, 2) no crush with stimulation, 3) crush and without stimulation, and 4) crush with stimula-tion. After euthanasia, the optic nerves were collected for lipidomic analysis. The Bligh and Dyer method was used for lipid extraction, followed by mass spectrometry lipid profil-ing with a Q-Exactive Orbitrap Liquid Chromatography-Mass Spectrometer (LC MS-MS). The raw scans were analysed with LipidSearch 4.1.3 and the statistical analysis was con-ducted through Metaboanalyst 4.0. (C) 2020 The Authors. Published by Elsevier Inc.