High Ca2+ Influx During Traumatic Brain Injury Leads to Caspase-1-Dependent Neuroinflammation and Cell Death View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2017-08

AUTHORS

P. M. Abdul-Muneer, Mathew Long, Adriano Andrea Conte, Vijayalakshmi Santhakumar, Bryan J. Pfister

ABSTRACT

We investigated the hypothesis that high Ca2+ influx during traumatic brain injury induces the activation of the caspase-1 enzyme, which triggers neuroinflammation and cell apoptosis in a cell culture model of neuronal stretch injury and an in vivo model of fluid percussion injury (FPI). We first established that stretch injury causes a rapid increase in the intracellular Ca2+ level, which activates interleukin-converting enzyme caspase-1. The increase in the intracellular Ca2+ level and subsequent caspase-1 activation culminates into neuroinflammation via the maturation of IL-1β. Further, we analyzed caspase-1-mediated apoptosis by TUNEL staining and PARP western blotting. The voltage-gated sodium channel blocker, tetrodotoxin, mitigated the stretch injury-induced neuroinflammation and subsequent apoptosis by blocking Ca2+ influx during the injury. The effect of tetrodotoxin was similar to the caspase-1 inhibitor, zYVAD-fmk, in neuronal culture. To validate the in vitro results, we demonstrated an increase in caspase-1 activity, neuroinflammation and neurodegeneration in fluid percussion-injured animals. Our data suggest that neuronal injury/traumatic brain injury (TBI) can induce a high influx of Ca2+ to the cells that cause neuroinflammation and cell death by activating caspase-1, IL-1β, and intrinsic apoptotic pathways. We conclude that excess IL-1β production and cell death may contribute to neuronal dysfunction and cognitive impairment associated with TBI. More... »

PAGES

3964-3975

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s12035-016-9949-4

    DOI

    http://dx.doi.org/10.1007/s12035-016-9949-4

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1051588444

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27289225


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