Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal Rats

Spina bifida, known more commonly as myelomeningocele, is a neural tube defect that results in herniation of the cerebellum through the foramen magnum into the central canal as part of the Chiari II malformation. Effects stemming from the herniated cerebellum and its metabolic profile have not been...

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Main Authors: Evan Thielen, Marc Oria, Miki Watanabe-Chailland, Kristin Lampe, Lindsey Romick-Rosendale, Jose L. Peiro
Format: Article
Language:English
Published: MDPI AG 2023-05-01
Series:Metabolites
Subjects:
Online Access:https://www.mdpi.com/2218-1989/13/5/670
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author Evan Thielen
Marc Oria
Miki Watanabe-Chailland
Kristin Lampe
Lindsey Romick-Rosendale
Jose L. Peiro
author_facet Evan Thielen
Marc Oria
Miki Watanabe-Chailland
Kristin Lampe
Lindsey Romick-Rosendale
Jose L. Peiro
author_sort Evan Thielen
collection DOAJ
description Spina bifida, known more commonly as myelomeningocele, is a neural tube defect that results in herniation of the cerebellum through the foramen magnum into the central canal as part of the Chiari II malformation. Effects stemming from the herniated cerebellum and its metabolic profile have not been extensively studied. The objective of this study is to examine the metabolic effects of this disease on the cerebellum in utero through the utilization of a retinoid acid-induced Spina bifida rat model. Analysis of this model at mid-late (day 15) and term (day 20) of gestation in comparison to both non-exposed and retinoic acid-exposed non-myelomeningocele controls, the observed metabolic changes suggest that mechanisms of oxidative stress and energy depletion are at play in this neuro tissue. These notable mechanisms are likely to result in further damage to neural tissue as the fetus grows and the compressed cerebellum develops and herniates more due to myelomeningocele.
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spelling doaj.art-47dea89730cd4eb6a57fdf9d3178c8ac2023-11-18T02:26:15ZengMDPI AGMetabolites2218-19892023-05-0113567010.3390/metabo13050670Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal RatsEvan Thielen0Marc Oria1Miki Watanabe-Chailland2Kristin Lampe3Lindsey Romick-Rosendale4Jose L. Peiro5The Center for Fetal and Placental Research, Division of Pediatric General and Thoracic Surgery, Cincinnati Children’s Hospital Medical Center (CCHMC), Cincinnati, OH 45229, USAThe Center for Fetal and Placental Research, Division of Pediatric General and Thoracic Surgery, Cincinnati Children’s Hospital Medical Center (CCHMC), Cincinnati, OH 45229, USANMR-Based Metabolomics Core, Division of Pathology and Laboratory Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USAThe Center for Fetal and Placental Research, Division of Pediatric General and Thoracic Surgery, Cincinnati Children’s Hospital Medical Center (CCHMC), Cincinnati, OH 45229, USANMR-Based Metabolomics Core, Division of Pathology and Laboratory Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USAThe Center for Fetal and Placental Research, Division of Pediatric General and Thoracic Surgery, Cincinnati Children’s Hospital Medical Center (CCHMC), Cincinnati, OH 45229, USASpina bifida, known more commonly as myelomeningocele, is a neural tube defect that results in herniation of the cerebellum through the foramen magnum into the central canal as part of the Chiari II malformation. Effects stemming from the herniated cerebellum and its metabolic profile have not been extensively studied. The objective of this study is to examine the metabolic effects of this disease on the cerebellum in utero through the utilization of a retinoid acid-induced Spina bifida rat model. Analysis of this model at mid-late (day 15) and term (day 20) of gestation in comparison to both non-exposed and retinoic acid-exposed non-myelomeningocele controls, the observed metabolic changes suggest that mechanisms of oxidative stress and energy depletion are at play in this neuro tissue. These notable mechanisms are likely to result in further damage to neural tissue as the fetus grows and the compressed cerebellum develops and herniates more due to myelomeningocele.https://www.mdpi.com/2218-1989/13/5/670metabolismSpina bifidamyelomeningocelechiari type IIcerebellumfetal rat
spellingShingle Evan Thielen
Marc Oria
Miki Watanabe-Chailland
Kristin Lampe
Lindsey Romick-Rosendale
Jose L. Peiro
Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal Rats
Metabolites
metabolism
Spina bifida
myelomeningocele
chiari type II
cerebellum
fetal rat
title Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal Rats
title_full Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal Rats
title_fullStr Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal Rats
title_full_unstemmed Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal Rats
title_short Non-Targeted Metabolic Profiling of Cerebellum in Spina Bifida Fetal Rats
title_sort non targeted metabolic profiling of cerebellum in spina bifida fetal rats
topic metabolism
Spina bifida
myelomeningocele
chiari type II
cerebellum
fetal rat
url https://www.mdpi.com/2218-1989/13/5/670
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