Summary of Study ST000963

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, 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.
University of Miami
DepartmentOphthalmology, Bascom Palmer Eye Institute
LaboratorySanjoy K. Bhattacharya Lab
Last NameBhattacharya
First NameSanjoy
Address900 NW 17th St, Miami, FL 33136, USA
Submit Date2018-04-17
Num Groups9
Total Subjects28
Num Males28
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2018-09-27
Release Version1
Sanjoy Bhattacharya Sanjoy Bhattacharya application/zip

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Treatment ID:TR001016
Treatment Summary:A rat model of inflammation-induced ON regeneration was established by intravitreal injection of a yeast cell wall preparation (Zymosan A) and a cell permeant CPT-cAMP, immediately after ON crush. Ten-week-old male Fischer rats were deeply anesthetized with inhaled isoflurane, and the eyes were treated with topical anesthetic (proparacaine HCl 0.5% ophthalmic) and a cycloplegic (tropicamide 0.5% ophthalmic) to reduce pain and assist with visualization of intravitreal injections. The left ON was exposed by blunt dissection through a temporal, fornix-based conjunctival incision and crushed for 10 seconds with Dumoxel #N5 self-closing forceps (Dumont, Montignez, Switzerland). Absence of injury to the retinal vascular supply was confirmed by post-crush funduscopic examination. Intravitreal injections (5 µL) of PBS vehicle or a suspension of finely ground, sterilized Zymosan A (Z4250; Sigma-Aldrich, St. Louis, MO, USA; 12.5 mg/mL) plus CPT-cAMP (C3912; Sigma-Aldrich, St. Louis, MO, USA; 100 µM) were performed with a pulled glass pipette attached to a Hamilton syringe on a manual micromanipulator. Injections were made 2 mm posterior to the limbus, and care was taken to prevent lens injury, choroidal hemorrhage, or retinal detachment. Absence of these intraocular adverse events was confirmed by fundoscopic examination. Conjunctival incisions were closed with 8-0 vicryl sutures and petrolatum ophthalmic ointment was applied to the ocular surface.