ArticleAnnals of clinical and translational neurology2014
HIP/PAP prevents excitotoxic neuronal death and promotes plasticity.
Article in Annals of clinical and translational neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
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- Antimicrobial protein REG3A regulates glucose homeostasis and insulin resistance in obese diabetic mice.Communications biology · 2023Article
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- Traumatic Brain Injury: An Age-Dependent View of Post-Traumatic Neuroinflammation and Its Treatment.Pharmaceutics · 2021Review
- Identification of protein targets for the antidepressant effects ofNeural regeneration research · 2020Article
- Reg-1α Promotes Differentiation of Cortical Progenitors via Its N-Terminal Active Domain.Frontiers in cell and developmental biology · 2020Article
- Current Evidence on Cell Death in Preterm Brain Injury in Human and Preclinical Models.Frontiers in cell and developmental biology · 2020Review
- Reversible lesion in the splenium of the corpus callosum.Brain and behavior · 2019Review
- Beneficial Effects of Remifentanil Against Excitotoxic Brain Damage in Newborn Mice.Frontiers in neurology · 2019Article
- Four Decades After the Discovery of Regenerating Islet-Derived (Reg) Proteins: Current Understanding and Challenges.Frontiers in cell and developmental biology · 2019Review
- PAP/REG3A favors perineural invasion in pancreatic adenocarcinoma and serves as a prognostic marker.Cellular and molecular life sciences : CMLS · 2017Article
- The Anti-Inflammatory Effects of the Small Molecule Pifithrin-µ on BV2 Microglia.Developmental neuroscience · 2015Article
Corrections and comments
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Authors and funding
18 authors at 11 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesExcitotoxicity plays a significant role in the pathogenesis of perinatal brain injuries. Among the consequences of excessive activation of the N-methyl-d-aspartate (NMDA)-type glutamate are oxidative stress caused by free radical release from damaged mitochondria, neuronal death and subsequent loss of connectivity. Drugs that could protect nervous tissue and support regeneration are attractive therapeutic options. The hepatocarcinoma intestine pancreas protein/pancreatitis-associated protein I (HIP/PAP) or Reg3α, which is approved for clinical testing for the protection and regeneration of the liver, is upregulated in the central nervous system following injury or disease. Here, we examined the neuroprotective/neuroregenerative potential of HIP/PAP following excitotoxic brain injury.
methodsWe studied the expression of HIP/PAP and two of its putative effectors, cAMP-regulated phosphoprotein 19 (ARPP19) and growth-associated protein 43 (GAP-43), in the neonatal brain, and the protective/regenerative properties of HIP/PAP in three paradigms of perinatal excitotoxicity: intracerebral injection of the NMDA agonist ibotenate in newborn pups, a pediatric model of traumatic brain injury, and cultured primary cortical neurons.
resultsHIP/PAP, ARPP19, and GAP-43 were expressed in the neonatal mouse brain. HIP/PAP prevented the formation of cortical and white matter lesions and reduced neuronal death and glial activation following excitotoxic insults in vivo. In vitro, HIP/PAP promoted neuronal survival, preserved neurite complexity and fasciculation, and protected cell contents from reactive oxygen species (ROS)-induced damage.
interpretationHIP/PAP has strong neuroprotective/neuroregenerative potential following excitotoxic injury to the developing brain, and could represent an interesting therapeutic strategy in perinatal brain injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.