Summary of Study ST003083
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 PR001918. The data can be accessed directly via it's Project DOI: 10.21228/M8ST6K 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 | ST003083 |
| Study Title | Metabolome changes in embryonic CSF (Part 5) |
| Study Summary | Targeted MS analysis of embryonic CSF at E14.5, 48 hours after Saline or PolyI:C injected into mother. |
| Institute | Boston Children's Hospital, Harvard Medical School |
| Laboratory | Kanarek Lab |
| Last Name | Petrova |
| First Name | Boryana |
| Address | Enders 1116.2 300 Longwood Ave |
| Boryana.Petrova@childrens.harvard.edu | |
| Phone | 6179197352 |
| Submit Date | 2024-01-16 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2024-03-01 |
| Release Version | 1 |
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Project:
| Project ID: | PR001918 |
| Project DOI: | doi: 10.21228/M8ST6K |
| Project Title: | Metabolomics of Mouse Embryonic CSF Following Maternal Immune Activation |
| Project Summary: | The embryonic cerebrospinal fluid (eCSF) is critical for the developing central nervous system (CNS), from neurogenesis to lifelong cognitive functions. Changes in eCSF composition due to inflammation can impact brain function. We recently identified an abnormal cytokine signature in eCSF following maternal immune activation (MIA), a mouse model of autism spectrum disorder (ASD). We hypothesized that MIA leads to other alterations in eCSF composition and employed untargeted metabolomics to profile changes in the eCSF metabolome in mice after inducing MIA with polyI:C. We report these data here as a resource, including a comprehensive MS1 and MS2 reference dataset, and present additional datasets comparing two mouse strains (CD-1 and C57Bl/6) and two developmental time points (E12.5 and E14.5). Targeted metabolomics further validated changes in eCSF upon MIA. We show a significant elevation of glucocorticoids and kynurenine pathway related metabolites. Both pathways are relevant for suppressing inflammation or could be informative as disease biomarkers. Our resource should inform future mechanistic studies regarding the etiology of MIA neuropathology and roles and contributions of eCSF metabolites to brain development. |
| Institute: | Boston Childrens Hospital |
| Last Name: | Petrova |
| First Name: | Boryana |
| Address: | 300 Longwood Av, Boston, MA, 2115, USA |
| Email: | boryana.petrova@childrens.harvard.edu |
| Phone: | 6173557433 |
