ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Mechanisms of mouse neural precursor expansion after neonatal hypoxia-ischemia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 40 citations in OpenAlex.
- Neuroplasticity After Hypoxic-Ischemic Brain Injury in Neonatal Pigs Based on Time-Dependent Behavior ofNeurochemical research · 2025Article
- Constraint-Induced Movement Therapy (CIMT) and Neural Precursor Cell (NPC) Transplantation Synergistically Promote Anatomical and Functional Recovery in a Hypoxic-Ischemic Mouse Model.International journal of molecular sciences · 2024Article
- Brain energy metabolism: A roadmap for future research.Journal of neurochemistry · 2024Review
- The Notch pathway regulates autophagy after hypoxic-ischemic injury and affects synaptic plasticity.Brain structure & function · 2023Article
- The Endocannabinoid System as a Target for Neuroprotection/Neuroregeneration in Perinatal Hypoxic-Ischemic Brain Injury.Biomedicines · 2022Review
- Induction of Nanog in neural progenitor cells for adaptive regeneration of ischemic brain.Experimental & molecular medicine · 2022Article
- Mechanisms of Tertiary Neurodegeneration after Neonatal Hypoxic-Ischemic Brain Damage.Pediatric medicine (Hong Kong, China) · 2022Article
- Analyzing mouse neural stem cell and progenitor cell proliferation using EdU incorporation and multicolor flow cytometry.STAR protocols · 2022Article
- Leukemia Inhibitory Factor Is Required for Subventricular Zone Astrocyte Progenitor Proliferation and for Prokineticin-2 Production after a Closed Head Injury in Mice.Neurotrauma reports · 2021Article
- Neuroregenerative and protective functions of Leukemia Inhibitory Factor in perinatal hypoxic-ischemic brain injury.Experimental neurology · 2020Article
- Developmental IL-6 Exposure Favors Production of PDGF-Responsive Multipotential Progenitors at the Expense of Neural Stem Cells and Other Progenitors.Stem cell reports · 2020Article
- Neonatal hypoxia-ischemia in rat elicits a region-specific neurotrophic response in SVZ microglia.Journal of neuroinflammation · 2020Article
- Stem Cell Therapy for Pediatric Traumatic Brain Injury.Frontiers in neurology · 2020Review
- MicroRNAs in brain development and cerebrovascular pathophysiology.American journal of physiology. Cell physiology · 2019Review
- Safety and efficacy of ex vivo expanded CD34Stem cell research & therapy · 2019Article
- Insulin-like Growth Factor II: An Essential Adult Stem Cell Niche Constituent in Brain and Intestine.Stem cell reports · 2019Article
- Neural stem cell therapies and hypoxic-ischemic brain injury.Progress in neurobiology · 2019Review
- Pediatric brain repair from endogenous neural stem cells of the subventricular zone.Pediatric research · 2018Review
- Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury.Journal of visualized experiments : JoVE · 2017Article
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6 authors at 2 institutions in 1 country.
Funding
Abstract
Neonatal hypoxia-ischemia (H-I) is the leading cause of brain damage resulting from birth complications. Studies in neonatal rats have shown that H-I acutely expands the numbers of neural precursors (NPs) within the subventricular zone (SVZ). The aim of these studies was to establish which NPs expand after H-I and to determine how leukemia inhibitory factor (LIF) insufficiency affects their response. During recovery from H-I, the number of Ki67(+) cells in the medial SVZ of the injured hemisphere increased. Similarly, the number and size of primary neurospheres produced from the injured SVZ increased approximately twofold versus controls, and, upon differentiation, more than twice as many neurospheres from the damaged brain were tripotential, suggesting an increase in neural stem cells (NSCs). However, multimarker flow cytometry for CD133/LeX/NG2/CD140a combined with EdU incorporation revealed that NSC frequency diminished after H-I, whereas that of two multipotential progenitors and three unique glial-restricted precursors expanded, attributable to changes in their proliferation. By quantitative PCR, interleukin-6, LIF, and CNTF mRNA increased but with significantly different time courses, with LIF expression correlating best with NP expansion. Therefore, we evaluated the NP response to H-I in LIF-haplodeficient mice. Flow cytometry revealed that one subset of multipotential and bipotential intermediate progenitors did not increase after H-I, whereas another subset was amplified. Altogether, our studies demonstrate that neonatal H-I alters the composition of the SVZ and that LIF is a key regulator for a subset of intermediate progenitors that expand during acute recovery from neonatal H-I.
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