Molecular and bioenergetic dynamics of in utero chronic hypoxia on placenta and brain

NIH RePORTER · NIH · R21 · $260,887 · view on reporter.nih.gov ↗

Abstract

PROJECT SUMMARY Insufficiency of the placenta due to conditions such as hypertension, diabetes, and fetal congenital heart disease can lead to chronic in utero hypoxia. Chronic hypoxia increases the risk of neurodevelopmental disorders by disrupting the "placenta-brain" axis. Furthermore, the effects of chronic hypoxia on the developing brain include disrupted energy metabolism and epigenome disruption, also called the metabolic-epigenetic axis. Rodent models of prenatal hypoxia are useful for studying the complex relationship between the placenta, brain, and epigenome. We developed 4D in utero Oxy-wavelet MRI (4D-uMRI) technology for simultaneous structural and temporal mitochondrial dynamics assessment. We applied this technique to elucidate the variable metabolic dynamics of multiple models of prenatal injury. We have additional expertise in modeling prenatal brain injury and analyzing the effects of injury on the molecular phenotype of the developing brain through single nucleus multi-omics. In this proposal, we will leverage our combined expertise to study the effects of chronic hypoxia on the placenta, brain, and epigenome. Our team has expertise in neuroscience, imaging, pathology, and placental biology. This study allows us to derive a comprehensive understanding of the correlation between metabolic profiling and molecular phenotype. We will compare normoxic litters to animals exposed to 11% inspired oxygen from embryonic day 14.5 to 17.5. In Aim 1, we will use 4D-uMRI studies to determine to examine the relationship between placental structural anomalies and brain structural and metabolic dysfunction from chronic hypoxia. The study will provide insight into whether there is a direct relationship between the extent of placental insufficiency and brain metabolic disruption and growth parameters. In Aim 2, we will assess the brain's metabolic response to hypoxia to test the relationship between the extent of metabolic dysfunction and disruption of the transcriptome and epigenome through single nucleus multi-omic sequencing. The study proposes an innovative approach to testing the correlation between the extent of metabolic disruption and molecular phenotype. Together, these experiments will allow us to recognize novel correlations between structure, function, and molecular disruption to discover novel targets for treating the neurodevelopmental deficits from chronic hypoxic brain injury.

Key facts

NIH application ID
10988582
Project number
1R21HD114071-01A1
Recipient
CHILDREN'S HOSP OF PHILADELPHIA
Principal Investigator
Ana Cristancho
Activity code
R21
Funding institute
NIH
Fiscal year
2024
Award amount
$260,887
Award type
1
Project period
2024-08-09 → 2026-07-31