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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MDPI AG
2023-05-01
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Series: | Metabolites |
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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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format | Article |
id | doaj.art-47dea89730cd4eb6a57fdf9d3178c8ac |
institution | Directory Open Access Journal |
issn | 2218-1989 |
language | English |
last_indexed | 2024-03-11T03:30:14Z |
publishDate | 2023-05-01 |
publisher | MDPI AG |
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series | Metabolites |
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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