Mecanismos biológicos involucrados en la propagación del daño en el traumatismo encéfalo craneano

Rovegno, Maximiliano; Soto, Paola; Sáez, Juan C.; Bernhardi, Rommy von

doi:10.1016/j.medin.2011.06.008

Cited by 34 publications

(15 citation statements)

References 72 publications

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“…Long-term neurological deficits from TBI are associated with neuroinflammation, and may aggravate over time to more severe secondary injuries, making prevention and treatment a very complex task [1], [11], [12], [13], [14]. Currently, a very well characterized TBI model for chronic brain atrophy, which addresses proximal and distal subcortical regions vulnerable to injury, is not available.…”

Section: Introductionmentioning

confidence: 99%

“…Unfortunately to date, many studies concentrate on specific subcortical regions, while others focus only on white matter, making it difficult to translate the findings on pathological mechanisms and therapies generated in TBI animal models to clinical applications [15], [16], [17], [18]. A better understanding of the neuropathology propagation associated with TBI, through investigations of neuro-inflammatory mechanisms will allow us to efficiently manage and treat the evolution of TBI-secondary neuropathologies and cognitive disabilities after the acute phase [11], [19]. In the present in vivo study, the neuro-inflammatory responses in subcortical regions, such as the dorsal striatum, thalamus, and white matter as corpus callosum, hippocampal fimbria-fornix, and cerebral peduncle were characterized in chronic TBI.…”

Section: Introductionmentioning

confidence: 99%

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Long-Term Upregulation of Inflammation and Suppression of Cell Proliferation in the Brain of Adult Rats Exposed to Traumatic Brain Injury Using the Controlled Cortical Impact Model

et al. 2013

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The long-term consequences of traumatic brain injury (TBI), specifically the detrimental effects of inflammation on the neurogenic niches, are not very well understood. In the present in vivo study, we examined the prolonged pathological outcomes of experimental TBI in different parts of the rat brain with special emphasis on inflammation and neurogenesis. Sixty days after moderate controlled cortical impact injury, adult Sprague-Dawley male rats were euthanized and brain tissues harvested. Antibodies against the activated microglial marker, OX6, the cell cycle-regulating protein marker, Ki67, and the immature neuronal marker, doublecortin, DCX, were used to estimate microglial activation, cell proliferation, and neuronal differentiation, respectively, in the subventricular zone (SVZ), subgranular zone (SGZ), striatum, thalamus, and cerebral peduncle. Stereology-based analyses revealed significant exacerbation of OX6-positive activated microglial cells in the striatum, thalamus, and cerebral peduncle. In parallel, significant decrements in Ki67-positive proliferating cells in SVZ and SGZ, but only trends of reduced DCX-positive immature neuronal cells in SVZ and SGZ were detected relative to sham control group. These results indicate a progressive deterioration of the TBI brain over time characterized by elevated inflammation and suppressed neurogenesis. Therapeutic intervention at the chronic stage of TBI may confer abrogation of these deleterious cell death processes.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Long-Term Upregulation of Inflammation and Suppression of Cell Proliferation in the Brain of Adult Rats Exposed to Traumatic Brain Injury Using the Controlled Cortical Impact Model

et al. 2013

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“…Hyperglycemia after severe TBI is associated with an increase in pro-inflammatory cytokines and pro-inflammatory transcription factors, such as transforming growth factor (TGF-β), interleukin 1β (IL1-β) and tumor necrosis factor-α (TNFα) [63, 64]. These cytokines increase significantly in the peripheral blood, cerebrospinal fluid, and brain tissue after TBI, which closely correlates with the severity and bad outcome of TBI patients [65].…”

Section: Hyperglycemia and Clinical Outcomes After Traumatic Brain Inmentioning

confidence: 99%

Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor

et al. 2016

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Hyperglycemia after severe traumatic brain injury (TBI) occurs frequently and is associated with poor clinical outcome and increased mortality. In this review, we highlight the mechanisms that lead to hyperglycemia and discuss how they may contribute to poor outcomes in patients with severe TBI. Moreover, we systematically review the proper management of hyperglycemia after TBI, covering topics such as nutritional support, glucose control, moderated hypothermia, naloxone, and mannitol treatment. However, to date, an optimal and safe glycemic target range has not been determined, and may not be safe to implement among TBI patients. Therefore, there is a mandate to explore a reasonable glycemic target range that can facilitate recovery after severe TBI.

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“…Activation of neuronal Panx1 channels by ATP and glutamate released through Cx43 HCs from astrocytes exposed to CM-A β was shown to induce neuronal death [126]. Therefore, it has been proposed that blockade of astroglia and/or neuronal Cx HCs and Panx1 channels of the inflamed nervous system may represent a strategy to reduce neuronal loss in various pathological states [157–159]. Additionally, the effect of the maternal environment on the developing CNS in the offspring has been analyzed in fetal nonhuman primates.…”

Section: CX Hcs and Panx1 Channels In Glial Cell And Mastocytesmentioning

confidence: 99%

Possible Involvement of TLRs and Hemichannels in Stress-Induced CNS Dysfunction via Mastocytes, and Glia Activation

Aguirre

Maturana

Harcha

et al. 2013

Mediators of Inflammation

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In the central nervous system (CNS), mastocytes and glial cells (microglia, astrocytes and oligodendrocytes) function as sensors of neuroinflammatory conditions, responding to stress triggers or becoming sensitized to subsequent proinflammatory challenges. The corticotropin-releasing hormone and glucocorticoids are critical players in stress-induced mastocyte degranulation and potentiation of glial inflammatory responses, respectively. Mastocytes and glial cells express different toll-like receptor (TLR) family members, and their activation via proinflammatory molecules can increase the expression of connexin hemichannels and pannexin channels in glial cells. These membrane pores are oligohexamers of the corresponding protein subunits located in the cell surface. They allow ATP release and Ca2+ influx, which are two important elements of inflammation. Consequently, activated microglia and astrocytes release ATP and glutamate, affecting myelinization, neuronal development, and survival. Binding of ligands to TLRs induces a cascade of intracellular events leading to activation of several transcription factors that regulate the expression of many genes involved in inflammation. During pregnancy, the previous responses promoted by viral infections and other proinflammatory conditions are common and might predispose the offspring to develop psychiatric disorders and neurological diseases. Such disorders could eventually be potentiated by stress and might be part of the etiopathogenesis of CNS dysfunctions including autism spectrum disorders and schizophrenia.

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Mecanismos biológicos involucrados en la propagación del daño en el traumatismo encéfalo craneano

Cited by 34 publications

References 72 publications

Long-Term Upregulation of Inflammation and Suppression of Cell Proliferation in the Brain of Adult Rats Exposed to Traumatic Brain Injury Using the Controlled Cortical Impact Model

Long-Term Upregulation of Inflammation and Suppression of Cell Proliferation in the Brain of Adult Rats Exposed to Traumatic Brain Injury Using the Controlled Cortical Impact Model

Review: Traumatic brain injury and hyperglycemia, a potentially modifiable risk factor

Possible Involvement of TLRs and Hemichannels in Stress-Induced CNS Dysfunction via Mastocytes, and Glia Activation

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