TY - JOUR
T1 - Mitochondrial lipid profiling data of a traumatic optic neuropathy model
AU - Nuesi, Ronaldo
AU - Gallo, Ryan A.
AU - Meehan, Sean D.
AU - Nahas, John V.
AU - Dvoriantchikova, Galina
AU - Pelaez, Daniel
AU - Bhattacharya, Sanjoy K.
N1 - Funding Information:
P30EY014801, an unrestricted grant from Research to Prevent Blindness to Bascom Palmer Eye Institute, and the Dr. Al-Rashid Orbital Research Center Endowment. Metabolomics workbench is an effort of NIH Common Fund's Metabolomics Data Repository and Coordinating Center supported by U2C DK119886.
Funding Information:
This work was supported in part by NIH grant U01EY027257, NIH Center Core Grant
Funding Information:
This work was supported in part by NIH grant U01EY027257, NIH Center Core Grant, P30EY014801, an unrestricted grant from Research to Prevent Blindness to Bascom Palmer Eye Institute, and the Dr. Al-Rashid Orbital Research Center Endowment. Metabolomics workbench is an effort of NIH Common Fund's Metabolomics Data Repository and Coordinating Center supported by U2C DK119886.
PY - 2020/6
Y1 - 2020/6
N2 - Traumatic optic neuropathy (TON) is a degenerative process that occurs in a subset of patients following blunt force trauma to the head. This condition is characterized by retinal ganglion cell (RGC) death and axon degeneration within the optic nerve [1]. At the cellular level, mitochondrial changes are associated with many optic neuropathies [2, 3]. Here, we provide a dataset demonstrating changes in the optic nerve mitochondrial lipid profile of a sonication-induced traumatic optic neuropathy (SI-TON) mouse model at 1, 7, and 14 days after injury. 32 C57BL/6J mice were separated into 4 groups (control, 1, 7, and 14 days) of 8, with 4 males and 4 females in each. Mice were exposed to sonication-induced trauma as described previously (by Tao et al) and optic nerves were harvested at 1, 7, or 14 days following injury [4]. Mitochondria were isolated from homogenized optic nerves and lipids were extracted. Extracted mitochondrial lipids were analysed with a Q-Exactive Orbitrap Liquid Chromatography-Mass Spectrometer (LC MS-MS). Further analysis of raw data was conducted with LipidSearch 4.1.3 and Metaboanalyst 4.0. This data is publicly available at the Metabolomics Workbench, http://www.metabolomicsworkbench.org (Project ID: PR000905).
AB - Traumatic optic neuropathy (TON) is a degenerative process that occurs in a subset of patients following blunt force trauma to the head. This condition is characterized by retinal ganglion cell (RGC) death and axon degeneration within the optic nerve [1]. At the cellular level, mitochondrial changes are associated with many optic neuropathies [2, 3]. Here, we provide a dataset demonstrating changes in the optic nerve mitochondrial lipid profile of a sonication-induced traumatic optic neuropathy (SI-TON) mouse model at 1, 7, and 14 days after injury. 32 C57BL/6J mice were separated into 4 groups (control, 1, 7, and 14 days) of 8, with 4 males and 4 females in each. Mice were exposed to sonication-induced trauma as described previously (by Tao et al) and optic nerves were harvested at 1, 7, or 14 days following injury [4]. Mitochondria were isolated from homogenized optic nerves and lipids were extracted. Extracted mitochondrial lipids were analysed with a Q-Exactive Orbitrap Liquid Chromatography-Mass Spectrometer (LC MS-MS). Further analysis of raw data was conducted with LipidSearch 4.1.3 and Metaboanalyst 4.0. This data is publicly available at the Metabolomics Workbench, http://www.metabolomicsworkbench.org (Project ID: PR000905).
KW - Lipidomics
KW - Liquid Chromatography-Mass Spectrometry
KW - Metabolomics
KW - Mitochondrial lipids
KW - Neurodegeneration
KW - Traumatic Optic Neuropathy
UR - http://www.scopus.com/inward/record.url?scp=85084448718&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85084448718&partnerID=8YFLogxK
U2 - 10.1016/j.dib.2020.105649
DO - 10.1016/j.dib.2020.105649
M3 - Article
AN - SCOPUS:85084448718
VL - 30
JO - Data in Brief
JF - Data in Brief
SN - 2352-3409
M1 - 105649
ER -