ArticleScientific reports2015
Bv8/prokineticin 2 is involved in Aβ-induced neurotoxicity.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Therapeutic Potential of Targeting Prokineticin Receptors in Diseases.Pharmacological reviews · 2023Review
- Effects of Prokineticins on Cerebral Cell Function and Blood-Brain Barrier Permeability.International journal of molecular sciences · 2023Article
- Blocking prokineticin receptors attenuates synovitis and joint destruction in collagen-induced arthritis.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Non-Peptide Agonists and Antagonists of the Prokineticin Receptors.Current issues in molecular biology · 2022Review
- Potential Clinical Role of Prokineticin 2 (PK2) in Neurodegenerative Diseases.Current neuropharmacology · 2022Article
- Alzheimer's disease-associated inflammatory pathways might contribute to osteoporosis through the interaction betweenFrontiers in neurology · 2022Article
- Prokineticin-2 prevents neuronal cell deaths in a model of traumatic brain injury.Nature communications · 2021Observational
- Evidence-Based View of Safety and Effectiveness of Prokineticin Receptors Antagonists during Pregnancy.Biomedicines · 2021Article
- The Role of Prokineticin 2 in Oxidative Stress and in Neuropathological Processes.Frontiers in pharmacology · 2021Review
- Circadian Rhythm Disruption and Alzheimer's Disease: The Dynamics of a Vicious Cycle.Current neuropharmacology · 2021Article
- 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
- Article
- Prokineticin signaling in heart-brain developmental axis: Therapeutic options for heart and brain injuries.Pharmacological research · 2020Review
- Roles of Prokineticin 2 in Subarachnoid Hemorrhage-Induced Early Brain Injury via Regulation of Phenotype Polarization in Astrocytes.Molecular neurobiology · 2020Article
- The overexpression of RBM3 alleviates TBI-induced behaviour impairment and AD-like tauopathy in mice.Journal of cellular and molecular medicine · 2020Article
- Prokineticin Receptor Inhibition With PC1 Protects Mouse Primary Sensory Neurons From Neurotoxic Effects of Chemotherapeutic DrugsFrontiers in immunology · 2020Article
- Article
- Chemokines in Alzheimer's Disease: New Insights Into Prokineticins, Chemokine-Like Proteins.Frontiers in pharmacology · 2019Review
- AD-Related N-Terminal Truncated Tau Is Sufficient to Recapitulate In Vivo the Early Perturbations of Human Neuropathology: Implications for Immunotherapy.Molecular neurobiology · 2018Article
- The McGill Transgenic Rat Model of Alzheimer's Disease Displays Cognitive and Motor Impairments, Changes in Anxiety and Social Behavior, and Altered Circadian Activity.Frontiers in aging neuroscience · 2018Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bv8/Prokineticin 2 (PROK2) is a bioactive peptide initially discovered as a regulator of gastrointestinal motility. Among multiple biological roles demonstrated for PROK2, it was recently established that PROK2 is an insult-inducible endangering mediator for cerebral damage. Aim of the present study was to evaluate the PROK2 and its receptors' potential involvement in amyloid beta (Aβ) neurotoxicity, a hallmark of Alzheimer's disease (AD) and various forms of traumatic brain injury (TBI). Analyzing primary cortical cultures (CNs) and cortex and hippocampus from Aβ treated rats, we found that PROK2 and its receptors PKR1 and PKR2 mRNA are up-regulated by Aβ, suggesting their potential involvement in AD. Hence we evaluated if impairing the prokineticin system activation might have protective effect against neuronal death induced by Aβ. We found that a PKR antagonist concentration-dependently protects CNs against Aβ(1-42)-induced neurotoxicity, by reducing the Aβ-induced PROK2 neuronal up-regulation. Moreover, the antagonist completely rescued LTP impairment in hippocampal slices from 6 month-old Tg2576 AD mice without affecting basal synaptic transmission and paired pulse-facilitation paradigms. These results indicate that PROK2 plays a role in cerebral amyloidosis and that PROK2 antagonists may represent a new approach for ameliorating the defining pathology of AD.
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