ArticleJournal of neurochemistry2012
Mechanisms of calpain mediated proteolysis of voltage gated sodium channel α-subunits following in vitro dynamic stretch injury.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 59 citations in OpenAlex.
- A 3D Human Neuron-on-Chip Platform to Monitor Neuronal Injury Responses.Advanced healthcare materials · 2026Article
- Article
- Mechanisms of Traumatic Spinal Cord Injury AIS Grade Conversion.Neurotrauma reports · 2025Review
- Experimental and computational evidence that Calpain-10 binds to the carboxy terminus of NaScientific reports · 2024Article
- Identifying the Phenotypes of Diffuse Axonal Injury Following Traumatic Brain Injury.Brain sciences · 2023Review
- Neuronal RBM5 modulates cell signaling responses to traumatic and hypoxic-ischemic injury in a sex-dependent manner.Cell death discovery · 2023Article
- Unraveling axonal mechanisms of traumatic brain injury.Acta neuropathologica communications · 2022Article
- Real time imaging of intra-axonal calcium flux in an explant mouse model of axonal Guillain-Barré syndrome.Experimental neurology · 2022Article
- Dynamic Gain Analysis Reveals Encoding Deficiencies in Cortical Neurons That Recover from Hypoxia-Induced Spreading Depolarizations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Modelling human pathology of traumatic brain injury in animal models.Journal of internal medicine · 2019Review
- Blood Biomarkers for Traumatic Brain Injury: A Quantitative Assessment of Diagnostic and Prognostic Accuracy.Frontiers in neurology · 2019Review
- MRI Evidence of Altered Callosal Sodium in Mild Traumatic Brain Injury.AJNR. American journal of neuroradiology · 2018Article
- PHLPP2 stabilization by p27 mediates its inhibition of bladder cancer invasion by promoting autophagic degradation of MMP2 protein.Oncogene · 2018Article
- Do sodium channel proteolytic fragments regulate sodium channel expression?Channels (Austin, Tex.) · 2017Article
- High CaMolecular neurobiology · 2017Article
- Update on fluid biomarkers for concussion.Concussion (London, England) · 2016Review
- Stretch Injury of Human Induced Pluripotent Stem Cell Derived Neurons in a 96 Well Format.Scientific reports · 2016Article
- The role of stretch-activated ion channels in acute respiratory distress syndrome: finally a new target?American journal of physiology. Lung cellular and molecular physiology · 2016Review
- An update on transcriptional and post-translational regulation of brain voltage-gated sodium channels.Amino acids · 2016Review
- Neuromechanics and Pathophysiology of Diffuse Axonal Injury in Concussion.Bridge (Washington, D.C. : 1969) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Although enhanced calpain activity is well documented after traumatic brain injury (TBI), the pathways targeting specific substrate proteolysis are less defined. Our past work demonstrated that calpain cleaves voltage gated sodium channel (NaCh) α-subunits in an in vitro TBI model. In this study, we investigated the pathways leading to NaCh cleavage utilizing our previously characterized in vitro TBI model, and determined the location of calpain activation within neuronal regions following stretch injury to micropatterned cultures. Calpain specific breakdown products of α-spectrin appeared within axonal, dendritic, and somatic regions 6 h after injury, concurrent with the appearance of NaCh α-subunit proteolysis in both whole cell or enriched axonal preparations. Direct pharmacological activation of either NMDA receptors (NMDArs) or NaChs resulted in NaCh proteolysis. Likewise, a chronic (6 h) dual inhibition of NMDArs/NaChs but not L-type voltage gated calcium channels significantly reduced NaCh proteolysis 6 h after mechanical injury. Interestingly, an early, transient (30 min) inhibition of NMDArs alone significantly reduced NaCh proteolysis. Although a chronic inhibition of calpain significantly reduced proteolysis, a transient inhibition of calpain immediately after injury failed to significantly attenuate NaCh proteolysis. These data suggest that both NMDArs and NaChs are key contributors to calpain activation after mechanical injury, and that a larger temporal window of sustained calpain activation needs consideration in developing effective treatments for TBI.
Indexed as
Identifiers
What OpenQuestion holds
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.