Cited by 43Traumatic Brain Injury and Neurovascular DisturbancesBarrier Structure and Function StudiesTraumatic Brain Injury Research

Acute traumatic brain injury-induced neuroinflammatory response and neurovascular disorders in the brain

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Kempuraj, Duraisamy, Ahmed, Mohammad Ejaz, Selvakumar, Govindhasamy Pushpavathi, Thangavel, Ramasamy, Raikwar, Sudhanshu P., Zaheer, Smita A., Iyer, Shankar S., Govindarajan, Raghav +4 more·2021·Neurotoxicity Research

Abstract

Acute traumatic brain injury (TBI) leads to neuroinflammation, neurodegeneration, cognitive decline, psychological disorders, increased blood-brain barrier (BBB) permeability, and microvascular damage in the brain. Inflammatory mediators secreted from activated glial cells, neurons, and mast cells are implicated in the pathogenesis of TBI through secondary brain damage. Abnormalities or damage to the neurovascular unit is the indication of secondary injuries in the brain after TBI. However, the precise mechanisms of molecular and ultrastructural neurovascular alterations involved in the pathogenesis of acute TBI are not yet clearly understood. Moreover, currently, there are no precision-targeted effective treatment options to prevent the sequelae of TBI. In this study, mice were subjected to closed head weight-drop-induced acute TBI and evaluated neuroinflammatory and neurovascular alterations in the brain by immunofluorescence staining or quantitation by enzyme-linked immunosorbent assay (ELISA) procedure. Mast cell stabilizer drug cromolyn was administered to inhibit the neuroinflammatory response of TBI. Results indicate decreased level of pericyte marker platelet-derived growth factor receptor-beta (PDGFR-β) and BBB-associated tight junction proteins junctional adhesion molecule-A (JAM-A) and zonula occludens-1 (ZO-1) in the brains 7 days after weight-drop-induced acute TBI as compared with the brains from sham control mice indicating acute TBI-associated BBB/tight junction protein disruption. Further, the administration of cromolyn drug significantly inhibited acute TBI-associated decrease of PDGFR-β, JAM-A, and ZO-1 in the brain. These findings suggest that acute TBI causes BBB/tight junction damage and that cromolyn administration could protect this acute TBI-induced brain damage as well as its long-time consequences.

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  • After TBI, loss of myelination can trigger neuroinflammation and upregulation of SGK1 transcription levels in oligodendrocytes.

    “After TBI, the loss of myelination can trigger neuroinflammation and upregulation of SGK1 transcription levels in oligodendrocytes”

    From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Kempuraj et al., 2021

    The Discussion (page unavailable) says TBI-related brain damage can lead to neuroinflammatory responses. It does not say that loss of myelination triggers those responses, or report increased SGK1 transcription in oligodendrocytes; searches for SGK1 and myelination found no supporting passage. (LLM, conf=0.86)

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Authors
Kempuraj, D., Ahmed, M. E., Selvakumar, G. P., Thangavel, R., Raikwar, S. P., Zaheer, S. A., Iyer, S. S., Govindarajan, R., Nattanmai Chandrasekaran, P., Burton, C., James, D., & Zaheer, A.
Affiliations
  • United States Department of Veterans Affairs (US)
  • University of Missouri (US)
  • Phelps County Regional Medical Center (US)
Corresponding author
  • Kempuraj, Duraisamy
  • Zaheer, Asgar
Venue
Neurotoxicity Research
Published
2020-09-21
Volume
39
Issue
2
Pages
359-368
ISSN
  • 1029-8428 (ISSN-L)
  • 1476-3524
OpenAlex
W3087366098
Cited by
43
References
72
Citations by year
2026: 2 · 2025: 5 · 2024: 15 · 2023: 7 · 2022: 6 · 2021: 7 · 2020: 1
FWCI
2.27
Type
journal article
Language
en
Open access
Locations
  • Neurotoxicity Research (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Leonard Wood Institute (W911NF-14-2-0034.)
  • National Institutes of Health (AG048205)
  • VA (Research Career Scientist Award)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
Keywords
acute traumatic brain injury, neuroinflammation, neurovascular unit, blood-brain barrier permeability, tight junction proteins, pericytes, PDGFRβ, JAM-A, ZO-1, mast cell stabilizers, disodium cromoglycate, secondary brain injury, weight-drop injury, neuroprotection
MeSH terms
Brain Injuries, Traumatic, Animals, Brain, Cerebrovascular Disorders, Encephalitis, Male, Neurons, Mice

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