ArticleJournal of molecular neuroscience : MN2012
Increased expression of calcium/calmodulin-dependent protein kinase type II subunit δ after rat traumatic brain injury.
Article in Journal of molecular neuroscience : MN, 2012. 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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18 citing papers in PubMed, 30 citations in OpenAlex.
- Research advances on CaMKs-mediated neurodevelopmental injury.Archives of toxicology · 2024Review
- Calcium and Non-Penetrating Traumatic Brain Injury: A Proposal for the Implementation of an Early Therapeutic Treatment for Initial Head Insults.Biomolecules · 2024Review
- Role of CaFrontiers in molecular neuroscience · 2022Review
- Potential Neuroprotective Mechanisms of Methamphetamine Treatment in Traumatic Brain Injury Defined by Large-Scale IonStar-Based Quantitative Proteomics.International journal of molecular sciences · 2021Article
- Chrysin attenuates traumatic brain injury-induced recognition memory decline, and anxiety/depression-like behaviors in rats: Insights into underlying mechanisms.Psychopharmacology · 2020Article
- Allopregnanolone Modulates GABAAR-Dependent CaMKIIδ3 and BDNF to Protect SH-SY5Y Cells Against 6-OHDA-Induced Damage.Frontiers in cellular neuroscience · 2019Article
- CaMKII Isoforms in Learning and Memory: Localization and Function.Frontiers in molecular neuroscience · 2018Review
- Proteomic Profiling of Mouse Brains Exposed to Blast-Induced Mild Traumatic Brain Injury Reveals Changes in Axonal Proteins and Phosphorylated Tau.Journal of Alzheimer's disease : JAD · 2018Article
- Long non-coding RNA C2dat1 regulates CaMKIIδ expression to promote neuronal survival through the NF-κB signaling pathway following cerebral ischemia.Cell death & disease · 2016Article
- [Traumatic brain injury].Der Nervenarzt · 2016Review
- Addiction-related genes in gambling disorders: new insights from parallel human and pre-clinical models.Molecular psychiatry · 2015Article
- The effects of BMSCs transplantation on autophagy by CX43 in the hippocampus following traumatic brain injury in rats.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014Article
- Phenoxybenzamine is neuroprotective in a rat model of severe traumatic brain injury.International journal of molecular sciences · 2014Article
- Hydrogen sulfide offers neuroprotection on traumatic brain injury in parallel with reduced apoptosis and autophagy in mice.PloS one · 2014Article
- The expression changes of cystathionine-β-synthase in brain cortex after traumatic brain injury.Journal of molecular neuroscience : MN · 2013Article
- Dynamic change of hydrogen sulfide after traumatic brain injury and its effect in mice.Neurochemical research · 2013Article
- Altered calcium signaling following traumatic brain injury.Frontiers in pharmacology · 2012Article
- Hypocalcemia as a prognostic factor in mortality and morbidity in moderate and severe traumatic brain injury.Asian journal of neurosurgeryArticle
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many cellular responses to Ca(2+) signals are mediated by Ca(2+)/calmodulin-dependent enzymes, among which is the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). CaMKII was originally described in rat brain tissue. In rat brain, four different subunits of the kinase have been identified: α, β, γ, and δ. This study aims to investigate changes of CaMKIIδ after traumatic brain injury and its possible role. Rat traumatic brain injury (TBI) model was established by controlled cortical injury system. In the present study, we mainly investigated the expression and cellular localization of CaMKIIδ after traumatic brain injury. Western blot analysis revealed that CaMKIIδ was present in normal rat brain cortex. It gradually increased, reached a peak at the third day after TBI, and then decreased. Importantly, more CaMKIIδ was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3.Importantly, immunohistochemistry analysis revealed that injury-induced expression of CaMKIIδ was colabeled by caspase-3 (apoptosis cells marker). Moreover, pretreatment with the CaMKII inhibitor (KN62) reduced the injury-induced activation of caspase-3. Noticeably, the CaMKII inhibitor KN-62 could reduce TBI-induced cell injury assessed with lesion volume and attenuate behavioral outcome evaluated by motor test. These data suggested that CaMKIIδ may be implicated in the apoptosis of neuron and the recovery of neurological outcomes. However, the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of CaMKIIδ after brain injury.
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