ArticleASN neuro2013
Egr-1 is a critical regulator of EGF-receptor-mediated expansion of subventricular zone neural stem cells and progenitors during recovery from hypoxia-hypoglycemia.
Article in ASN neuro, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Modeling Prenatal Immune Activation in Human Brain Organoids Uncovers IL-6-Dependent Interneuron Dysmaturation.bioRxiv : the preprint server for biology · 2026Article
- Heart failure impairs mood and memory in male rats and down-regulates the expression of numerous genes important for synaptic plasticity in related brain regions.Behavioural brain research · 2021Article
- TransSynW: A single-cell RNA-sequencing based web application to guide cell conversion experiments.Stem cells translational medicine · 2021Article
- Transcriptional regulation of adult neural stem/progenitor cells: tales from the subventricular zone.Neural regeneration research · 2020Review
- Regulation of embryonic and adult neurogenesis by Ars2.Development (Cambridge, England) · 2020Article
- miR‑92a‑3p regulates trypsinogen activation via Egr1 in AR42J cells.Molecular medicine reports · 2019Article
- Potential biomarkers for neuroinflammation and neurodegeneration at short and long term after neonatal hypoxic-ischemic insult in rat.Journal of neuroinflammation · 2019Article
- Pediatric brain repair from endogenous neural stem cells of the subventricular zone.Pediatric research · 2018Review
- Astrocyte-produced leukemia inhibitory factor expands the neural stem/progenitor pool following perinatal hypoxia-ischemia.Journal of neuroscience research · 2016Article
- Mechanisms of mouse neural precursor expansion after neonatal hypoxia-ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We recently established that the EGF-R (epidermal growth factor receptor) (EGF-R) is an essential regulator of the reactive expansion of SVZ (subventricular zone) NPs (neural precursors) that occurs during recovery from hypoxic-ischemic brain injury. The purpose of the current studies was to identify the conditions and the transcription factor (s) responsible for inducing the EGF-R. Here, we show that the increase in EGF-R expression and the more rapid division of the NPs can be recapitulated in in vitro by exposing SVZ NPs to hypoxia and hypoglycemia simultaneously, but not separately. The EGF-R promoter has binding sites for multiple transcription factors that includes the zinc finger transcription factor, Egr-1. We show that Egr-1 expression increases in NPs, but not astrocytes, following hypoxia and hypoglycemia where it accumulates in the nucleus. To determine whether Egr-1 is necessary for EGF-R expression, we used SiRNAs (small interfering RNA) specific for Egr-1 to decrease Egr-1 expression. Knocking-down Egr-1 decreased basal levels of EGF-R and it abolished the stress-induced increase in EGF-R expression. By contrast, HIF-1 accumulation did not contribute to EGF-R expression and FGF-2 only modestly induced EGF-R. These studies establish a new role for Egr-1 in regulating the expression of the mitogenic EGF-R. They also provide new information into mechanisms that promote NP expansion and provide insights into strategies for amplifying the numbers of stem cells for CNS (central nervous system) regeneration.
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