Erythropoietin-mediated neuroprotection in a pediatric mouse model of chronic hypoxia
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Updated: Apr 14, 2026
Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury
Published on: November 24, 2017
Eugene Chung1, Xiangmei Kong2, Mark P Goldberg2
1Department of Anesthesiology, University of Texas Southwestern Medical Center Harry Hines Blvd., Dallas, TX 75390, USA.
Insights
Chronic hypoxia impairs hippocampal neurogenesis and myelination in developing mice. Erythropoietin (EPO) therapy rescues neurogenesis and oligodendrocyte progenitor cells but not mature myelin loss.
Area of Science:
- Neuroscience
- Developmental Biology
- Pediatric Medicine
Background:
- Chronic hypoxia (CH) is a critical condition affecting pediatric morbidity and mortality.
- CH impacts hippocampal development and cortical myelination during crucial early life periods.
- Impaired hippocampal neurogenesis can lead to long-term cognitive deficits.
Purpose of the Study:
- To investigate the effects of erythropoietin (EPO) therapy on hippocampal neurogenesis and myelination in a pediatric model of CH.
- To determine if EPO can mitigate the negative impacts of CH on developing brain structures.
Main Methods:
- Utilized a pediatric mouse model subjected to chronic hypoxia.
- Assessed hippocampal neurogenesis by quantifying progenitor cells and actively dividing cells.
- Evaluated cortical oligodendrocyte progenitor (OPC) populations and myelination status.
- Administered EPO therapy to a subset of hypoxic mice.
Main Results:
- CH significantly decreased hippocampal neurogenesis, affecting early and late progenitors and actively dividing cells.
- EPO treatment rescued the observed decrease in hippocampal neurogenesis.
- CH reduced OPC populations in the cortex, leading to defective myelination.
- EPO therapy successfully rescued OPC populations but did not restore the loss of mature myelin.
Conclusions:
- Developing mice exposed to CH exhibit significant deficits in hippocampal neurogenesis and OPC populations.
- EPO therapy demonstrates potential in rescuing CH-induced impairments in hippocampal neurogenesis and OPCs.
- Further research is warranted to explore EPO's neuroprotective role in at-risk pediatric populations.
Abstract:
Chronic hypoxia (CH), a disease state that accounts for significant morbidity and mortality in pediatrics, occurs in many children during critical periods of hippocampal development and cortical myelination. Hippocampal neurogenesis occurs throughout postnatal life and is important for normal development, thus impairment results in long-term cognitive deficits. Erythropoietin (EPO), a drug commonly known for its role in erythrogenesis, has recently been evaluated in neuroprotection in neonatal injury models and preterm brain injury. However, the effects of EPO therapy on hippocampal neurogenesis and myelination in pediatric CH are unknown. We show that CH decreases hippocampal neurogenesis in a pediatric mouse model. This decrease in early and late progenitors, and actively dividing cells is rescued with EPO treatment. Furthermore, we show that CH during this critical time decreases oligodendrocyte progenitor (OPC) populations in the cortex, leading to defective myelination. However, EPO therapy is only able to rescue the OPC but not the loss of mature myelin. Overall, our findings demonstrate that CH in developing mice has significant effects on hippocampal neurogenesis and OPCs, which can be rescued with EPO treatment. Future studies should confirm the role of this FDA-approved therapy in neuroprotection in at-risk pediatric populations.
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