Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor alpha (TNFα) release in a rat brain

Lucca, Jurandir J. Dalle; Chavko, M; Dubick, Michael A.; Adeeb, Saleena; Falabella, Michael; Slack, Jessica L.; McCarron, Richard M.; Li, Yansong

doi:10.1016/j.jns.2012.02.002

Cited by 49 publications

(45 citation statements)

References 34 publications

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“…The need for improved therapeutics is particularly clear in the military in which evacuation of blast-exposed troops is often delayed by hours to several days due to the nature of conflict. As such, secondary responses within the brain often occur and may represent a potential target as described previously (Dalle Lucca et al, 2012).…”

Section: Discussionmentioning

confidence: 98%

Modeling clinically relevant blast parameters based on scaling principles produces functional & histological deficits in rats

Turner

Naser

Logsdon

et al. 2013

Experimental Neurology

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Section: Discussionmentioning

confidence: 98%

Modeling clinically relevant blast parameters based on scaling principles produces functional & histological deficits in rats

Turner

Naser

Logsdon

et al. 2013

Experimental Neurology

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“…OPN normalization by 7d points to an inflammatory role supporting acute degeneration. Other cytokines also increase after human TBI (Helmy et al, 2011), and with rodent impact acceleration (Shohami et al, 1994), fluid percussion (Vitarbo et al, 2004), cortical impact (Kelso et al, 2011), and blast neurotrauma (Dalle Lucca et al, 2012). While TBI OPN studies are limited, OPN rise with inflammation after cortical impact (von Gertten et al, 2005; Israelsson et al, 2006), cryolesion (Shin et al, 2005), and stab wound (Plantman, 2012) are documented.…”

Section: Discussionmentioning

confidence: 99%

Osteopontin expression in acute immune response mediates hippocampal synaptogenesis and adaptive outcome following cortical brain injury

Chan

Reeves

Phillips

2014

Experimental Neurology

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Traumatic brain injury (TBI) produces axotomy, deafferentation and reactive synaptogenesis. Inflammation influences synaptic repair, and the novel brain cytokine osteopontin (OPN) has potential to support axon regeneration through exposure of its integrin receptor binding sites. This study explored whether OPN secretion and proteolysis by matrix metalloproteinases (MMPs) mediate the initial degenerative phase of synaptogenesis, targeting reactive neuroglia to affect successful repair. Adult rats received unilateral entorhinal cortex lesion (UEC) modeling adaptive synaptic plasticity. Over the first week postinjury, hippocampal OPN protein and mRNA were assayed and histology performed. At 1–2d, OPN protein increased up to 51 fold, and was localized within activated, mobilized glia. OPN transcript also increased over 50 fold, predominantly within reactive microglia. OPN fragments known to be derived from MMP proteolysis were elevated at 1d, consistent with prior reports of UEC glial activation and enzyme production. Postinjury minocycline immunosuppression attenuated MMP-9 gelatinase activity, which was correlated with reduction of neutrophil gelatinase-associated lipocalin (LCN2) expression, and reduced OPN fragment generation. The antibiotic also attenuated removal of synapsin-1 positive axons from the deafferented zone. OPN KO mice subjected to UEC had similar reduction of hippocampal MMP-9 activity, as well as lower synapsin-1 breakdown over the deafferented zone. MAP1B and N-cadherin, surrogates of cytoarchitecture and synaptic adhesion, were not affected. OPN KO mice with UEC exhibited time dependent cognitive deficits during the synaptogenic phase of recovery. This study demonstrates that OPN can mediate immune response during TBI synaptic repair, positively influencing synapse reorganization and functional recovery.

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“…The pattern of brain damage corresponds with the detailed analysis of brain histopathology previously described in the same blast model [22]. …”

Section: Resultsmentioning

confidence: 96%

“…The upregulation of AQP-4, a water-channel protein, has been shown to facilitate cerebral cytotoxic edema formation in several TBI models [22–24]. After exposure to BOP, AQP-4 expression was significantly increased in cortex of both BOP exposed groups compared with the control group (Figures 3(a) and 3(b)).…”

Section: Resultsmentioning

confidence: 98%

Protection against Blast-Induced Traumatic Brain Injury by Increase in Brain Volume

Kawoos

McCarron

et al. 2017

BioMed Research International

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Blast-induced traumatic brain injury (bTBI) is a leading cause of injuries in recent military conflicts and it is responsible for an increased number of civilian casualties by terrorist attacks. bTBI includes a variety of neuropathological changes depending on the intensity of blast overpressure (BOP) such as brain edema, neuronal degeneration, diffuse axonal damage, and vascular dysfunction with neurological manifestations of psychological and cognitive abnormalities. Internal jugular vein (IJV) compression is known to reduce intracranial compliance by causing an increase in brain volume and was shown to reduce brain damage during closed impact-induced TBI. We investigated whether IJV compression can attenuate signs of TBI in rats after exposure to BOP. Animals were exposed to three 110 ± 5 kPa BOPs separated by 30 min intervals. Exposure to BOP resulted in a significant decrease of neuronal nuclei (NeuN) together with upregulation of aquaporin-4 (AQP-4), 3-nitrotyrosine (3-NT), and endothelin 1 receptor A (ETRA) expression in frontal cortex and hippocampus one day following exposures. IJV compression attenuated this BOP-induced increase in 3-NT in cortex and ameliorated the upregulation of AQP-4 in hippocampus. These results suggest that elevated intracranial pressure and intracerebral volume have neuroprotective potential in blast-induced TBI.

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Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor alpha (TNFα) release in a rat brain

Cited by 49 publications

References 34 publications

Modeling clinically relevant blast parameters based on scaling principles produces functional & histological deficits in rats

Modeling clinically relevant blast parameters based on scaling principles produces functional & histological deficits in rats

Osteopontin expression in acute immune response mediates hippocampal synaptogenesis and adaptive outcome following cortical brain injury

Protection against Blast-Induced Traumatic Brain Injury by Increase in Brain Volume

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