Summary of Study ST002047
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 PR001294. The data can be accessed directly via it's Project DOI: 10.21228/M8FQ39 This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
Study ID | ST002047 |
Study Title | Lyso-lipid induced oligodendrocytes maturation underlie restoration of optic nerve function |
Study Summary | Protein hyper-deimination and deficiency of lyso-phospholipids (LPC 18:1) has been associated with the pathology of demyelinating disease in both humans and mice. We uncovered interesting biology of LPC 18:1, in which LPC 18:1 induced optic nerve function restoration through oligodendrocyte maturation and remyelination in mouse model systems. Our in vitro studies show LPC 18:1 protection against neuron-ectopic hyper-deimination and stimulation of oligodendrocyte maturation, while in vivo investigations recorded optic nerve function improvement following optic nerve injections of LPC 18:1, in contrast to LPC 18:0. Thus just a change in a single bond renders a dramatic alternation in biological function. The incorporation of isobaric C13-histidine in newly synthesized myelin proteins and quantitative proteome shifts are consistent with remyelination underlying restoration in optic nerve function. These results suggest that exogenous LPC 18:1 may provide a therapeutic avenue for stemming vision loss in demyelinating diseases. |
Institute | University of Miami |
Last Name | Bhattacharya |
First Name | Sanjoy K. |
Address | 1638 NW 10th Avenue, Room 706-A, Miami, FL 33136 |
sbhattacharya@med.miami.edu | |
Phone | 3054824103 |
Submit Date | 2021-12-16 |
Raw Data Available | Yes |
Raw Data File Type(s) | raw(Thermo) |
Analysis Type Detail | LC-MS |
Release Date | 2022-01-21 |
Release Version | 1 |
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Project:
Project ID: | PR001294 |
Project DOI: | doi: 10.21228/M8FQ39 |
Project Title: | Lyso-lipid induced oligodendrocytes maturation underlie restoration of optic nerve function |
Project Summary: | Protein hyper-deimination and deficiency of lyso-phospholipids (LPC 18:1) has been associated with the pathology of demyelinating disease in both humans and mice. We uncovered interesting biology of LPC 18:1, in which LPC 18:1 induced optic nerve function restoration through oligodendrocyte maturation and remyelination in mouse model systems. Our in vitro studies show LPC 18:1 protection against neuron-ectopic hyper-deimination and stimulation of oligodendrocyte maturation, while in vivo investigations recorded optic nerve function improvement following optic nerve injections of LPC 18:1, in contrast to LPC 18:0. Thus just a change in a single bond renders a dramatic alternation in biological function. The incorporation of isobaric C13-histidine in newly synthesized myelin proteins and quantitative proteome shifts are consistent with remyelination underlying restoration in optic nerve function. These results suggest that exogenous LPC 18:1 may provide a therapeutic avenue for stemming vision loss in demyelinating diseases. |
Institute: | University of Miami |
Department: | Ophthalmology |
Last Name: | Bhattacharya |
First Name: | Sanjoy K. |
Address: | 1638 NW 10th Avenue, Room 706-A, Miami, FL 33136 |
Email: | sbhattacharya@med.miami.edu |
Phone: | 3054824103 |