Summary of study ST000963

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000661. The data can be accessed directly via it's Project DOI: 10.21228/M87D53 This work is supported by NIH grant, U2C- DK119886.

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Study IDST000963
Study TitleLipidomics of inflammation-induced optic nerve regeneration
Study Typeuntargeted LC-MS/MS profiling
Study SummaryIn adult mammals, retinal ganglion cells (RGCs) fail to regenerate their axons when damaged. As a result, RGCs die after acute injury and in progressive degenerative diseases such as glaucoma; such damage can lead to permanent vision loss and blindness. Little is known about the roles of lipids in axon injury and repair despite their fundamental importance in composition of cell membranes, myelin sheaths and mediation of signaling pathways. Study of the lipidome in the biology of optic nerve (ON) regeneration has been largely neglected. A better understanding of the roles that lipids play in RGC biology may enhance understanding of RGC-related diseases and point to novel treatments. Established experimental models of ON regeneration allow exploration of molecular determinants of RGC axon regenerative success and failure. In this study, we used high-resolution liquid chromatography-tandem mass spectrometry to analyze lipidomic profiles of the ON and retina in an ON crush model with and without intravitreal Zymosan injections to enhance regeneration. Our results reveal profound remodeling of retina and ON lipidomes that occur after injury. In the retina, Zymosan treatment largely abrogates widespread lipidome alterations. In the ON, Zymosan induces lipid profiles that are distinct from those observed in naïve and vehicle-injected crush controls. We have identified a number of lipid species, classes and fatty acids that may be involved in the mechanisms of axon damage and repair. Lipids upregulated during RGC regeneration may be interesting candidates for further functional studies.
Institute
University of Miami
DepartmentOphthalmology, Bascom Palmer Eye Institute
LaboratorySanjoy K. Bhattacharya Lab
Last NameBhattacharya
First NameSanjoy
Address900 NW 17th St, Miami, FL 33136, USA
Emailsbhattacharya@med.miami.edu
Phone3054824103
Submit Date2018-04-17
Num Groups9
Total Subjects28
Num Males28
Raw Data AvailableYes
Raw Data File Type(s).Raw
Analysis Type DetailLC-MS
Release Date2018-09-27
Release Version1
Sanjoy Bhattacharya Sanjoy Bhattacharya
https://dx.doi.org/10.21228/M87D53
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000661
Project DOI:doi: 10.21228/M87D53
Project Title:Lipidomics of inflammation-induced optic nerve regeneration
Project Type:untargeted LC-MS/MS lipid profiling
Project Summary:In adult mammals, retinal ganglion cells (RGCs) fail to regenerate their axons when damaged. As a result, RGCs die after acute injury and in progressive degenerative diseases such as glaucoma; such damage can lead to permanent vision loss and blindness. Little is known about the roles of lipids in axon injury and repair despite their fundamental importance in composition of cell membranes, myelin sheaths and mediation of signaling pathways. Study of the lipidome in the biology of optic nerve (ON) regeneration has been largely neglected. A better understanding of the roles that lipids play in RGC biology may enhance understanding of RGC-related diseases and point to novel treatments. Established experimental models of ON regeneration allow exploration of molecular determinants of RGC axon regenerative success and failure. In this study, we used high-resolution liquid chromatography-tandem mass spectrometry to analyze lipidomic profiles of the ON and retina in an ON crush model with and without intravitreal Zymosan injections to enhance regeneration. Our results reveal profound remodeling of retina and ON lipidomes that occur after injury. In the retina, Zymosan treatment largely abrogates widespread lipidome alterations. In the ON, Zymosan induces lipid profiles that are distinct from those observed in naïve and vehicle-injected crush controls. We have identified a number of lipid species, classes and fatty acids that may be involved in the mechanisms of axon damage and repair. Lipids upregulated during RGC regeneration may be interesting candidates for further functional studies.
Institute:University of Miami
Department:Bascom Palmer Eye Insitute, Ophthalmology
Laboratory:Sanjoy K. Bhattacharya lab
Last Name:Bhattacharya
First Name:Sanjoy
Address:McKnight Vision Research Center, 900 NW 17th St, Miami, FL 33136, USA
Email:sbhattacharya@med.miami.edu
Phone:3054824103
Funding Source:This work was partly supported by a grant from Glaucoma Research Foundation, Payden Glaucoma Research Fund (UCLA), NIH grants U01 EY027257, EY14801, Department of Defense grant number W81XWH-15-1-0079 and an unrestricted grant each from Research to Prevent Blindness to the University of Miami and UCLA.
Contributors:Anna M. Trzeciecka, David T. Stark, Jacky M. K. Kwong, Maria C. Piqueras, Sanjoy K. Bhattacharya and Joseph Caprioli
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