ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2012
Kollidon VA64, a membrane-resealing agent, reduces histopathology and improves functional outcome after controlled cortical impact in mice.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pre-Clinical Testing of Therapies for Traumatic Brain Injury.Journal of neurotrauma · 2018Guideline
- The role of homogenization cycles and Poloxamer 188 on the quality of mitochondria isolated for use in mitochondrial transplantation therapy.Scientific reports · 2025Article
- Traumatic axonal injury (TAI): definitions, pathophysiology and imaging-a narrative review.Acta neurochirurgica · 2021Review
- Revisiting Traumatic Brain Injury: From Molecular Mechanisms to Therapeutic Interventions.Biomedicines · 2020Review
- Cardiac Muscle Membrane Stabilization in Myocardial Reperfusion Injury.JACC. Basic to translational science · 2019Review
- Neuronal Membrane Disruption Occurs Late Following Diffuse Brain Trauma in Rats and Involves a Subpopulation of NeuN Negative Cortical Neurons.Frontiers in neurology · 2019Article
- Targeting microthrombosis and neuroinflammation with vepoloxamer for therapeutic neuroprotection after traumatic brain injury.Neural regeneration research · 2018Article
- PEO-PPO Diblock Copolymers Protect Myoblasts from Hypo-Osmotic Stress In Vitro Dependent on Copolymer Size, Composition, and Architecture.Biomacromolecules · 2017Article
- Traumatic Axonal Injury: Mechanisms and Translational Opportunities.Trends in neurosciences · 2016Review
- Instant membrane resealing in nlrp3 inflammmasome activation of endothelial cells.Frontiers in bioscience (Landmark edition) · 2016Article
- Poloxamer 188 Attenuates Cerebral Hypoxia/Ischemia Injury in Parallel with Preventing Mitochondrial Membrane Permeabilization and Autophagic Activation.Journal of molecular neuroscience : MN · 2015Article
- Emerging therapies in traumatic brain injury.Seminars in neurology · 2015Review
- Apelin-13 attenuates traumatic brain injury-induced damage by suppressing autophagy.Neurochemical research · 2015Article
- Membrane resealing as a promising strategy for early treatment of neurotrauma.Neural regeneration research · 2014Article
- The pharmacokinetics and pharmacodynamics of Kollidon VA64 dissociate its protective effects from membrane resealing after controlled cortical impact in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- PEG-PDLLA micelle treatment improves axonal function of the corpus callosum following traumatic brain injury.Journal of neurotrauma · 2014Article
- Therapy development for diffuse axonal injury.Journal of neurotrauma · 2013Article
- Neuroprotection for ischemic stroke: moving past shortcomings and identifying promising directions.International journal of molecular sciences · 2013Review
- Poloxamer-188 attenuates TBI-induced blood-brain barrier damage leading to decreased brain edema and reduced cellular death.Neurochemical research · 2012Article
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Authors and funding
9 authors.
Funding
Abstract
Loss of plasma membrane integrity is a feature of acute cellular injury/death in vitro and in vivo. Plasmalemma-resealing agents are protective in acute central nervous system injury models, but their ability to reseal cell membranes in vivo has not been reported. Using a mouse controlled cortical impact (CCI) model, we found that propidium iodide-positive (PI+) cells pulse labeled at 6, 24, or 48 hours maintained a degenerative phenotype and disappeared from the injured brain by 7 days, suggesting that plasmalemma permeability is a biomarker of fatal cellular injury after CCI. Intravenous or intracerebroventricular administration of Kollidon VA64, poloxamer P188, or polyethylene glycol 8000 resealed injured cell membranes in vivo (P<0.05 versus vehicle or poloxamer P407). Kollidon VA64 (1 mmol/L, 500 μL) administered intravenously to mice 1 hour after CCI significantly reduced acute cellular degeneration, chronic brain tissue damage, brain edema, blood-brain barrier damage, and postinjury motor deficits (all P<0.05 versus vehicle). However, VA64 did not rescue pulse-labeled PI+ cells from eventual demise. We conclude that PI permeability within 48 hours of CCI is a biomarker of eventual cell death/loss. Kollidon VA64 reduces secondary damage after CCI by mechanisms other than or in addition to resealing permeable cells.
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