Mild traumatic brain injury increases vulnerability to cerebral ischemia in mice.
Inflammation
Metabolism
Reperfusion
Stroke
Traumatic brain injury
Vasculature
Journal
Experimental neurology
ISSN: 1090-2430
Titre abrégé: Exp Neurol
Pays: United States
ID NLM: 0370712
Informations de publication
Date de publication:
08 2021
08 2021
Historique:
received:
02
03
2021
revised:
15
04
2021
accepted:
12
05
2021
pubmed:
17
5
2021
medline:
12
10
2021
entrez:
16
5
2021
Statut:
ppublish
Résumé
Recent studies have reported that TBI is an independent risk factor for subsequent stroke. Here, we tested the hypothesis that TBI would exacerbate experimental stroke outcomes via alternations in neuroimmune and neurometabolic function. We performed a mild closed-head TBI and then one week later induced an experimental stroke in adult male mice. Mice that had previously experienced TBI exhibited larger infarcts, greater functional deficits, and more pronounced neuroinflammatory responses to stroke. We hypothesized that impairments in central metabolic physiology mediated poorer outcomes after TBI. To test this, we treated mice with the insulin sensitizing drug pioglitazone (Pio) after TBI. Pio prevented the exacerbation of ischemic outcomes induced by TBI and also blocked the induction of insulin insensitivity by TBI. However, tissue respiratory function was not improved by Pio. Finally, TBI altered microvascular responses including promoting vascular accumulation of serum proteins and significantly impairing blood flow during the reperfusion period after stroke, both of which were reversed by treatment with Pio. Thus, TBI appears to exacerbate ischemic outcomes by impairing metabolic and microvascular physiology. These data have important implications because TBI patients experience strokes at greater rates than individuals without a history of head injury, but these data suggest that those strokes may also cause greater tissue damage and functional impairments in that population.
Identifiants
pubmed: 33992581
pii: S0014-4886(21)00171-0
doi: 10.1016/j.expneurol.2021.113765
pmc: PMC8210428
mid: NIHMS1706224
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
113765Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM109098
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128485
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM132494
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM104942
Pays : United States
Organisme : NIA NIH HHS
ID : T32 AG052375
Pays : United States
Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
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