Inflammation and the neurovascular unit in the setting of focal cerebral ischemia

del Zoppo, G.J.

doi:10.1016/j.neuroscience.2008.08.028

Cited by 243Neuroinflammation and Neurodegeneration MechanismsBarrier Structure and Function StudiesAcute Ischemic Stroke Management

Inflammation and the neurovascular unit in the setting of focal cerebral ischemia

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del Zoppo, G.J.·2009·Neuroscience

DOI 10.1016/j.neuroscience.2008.08.028PMC PMC2665879

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Abstract

Responses to focal cerebral ischemia by neurons and adjacent microvessels are rapid, simultaneous, and topographically related. Recent observations indicate the simultaneous appearance of proteases by components of nearby microvessels that are also expressed by neurons in the ischemic territory, implying that the events could be coordinated. The structural relationship of neurons to their microvascular supply, the direct functional participation of glial cells, and the observation of a highly ordered microvessel-neuron response to ischemia suggest that these elements are arranged in and behave in a unitary fashion, the neurovascular unit. Their roles as a unit in the stimulation of cellular inflammation and the generation of inflammatory mediators during focal cerebral ischemia have not been explored yet. However, components of the neurovascular unit both generate and respond to these influences under the conditions of ischemia. Here we briefly explore the potential inter-relationships of the components of the neurovascular unit with respect to their potential roles in ischemia-induced inflammatory responses.

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The first phase of blood-brain barrier opening after ischemia/reperfusion is controlled by subtle endothelial cytoskeleton alterations 30-60 min after injury, followed later by enzymatic cleavage of tight junction proteins after inflammatory cell recruitment.
“The first phase is controlled by subtle endothelial cytoskeleton alterations 30-60 min after ischemia/reperfusion injury, followed later by enzymatic cleavage of TJ proteins after inflammatory cell recruitment (324, 534, 703).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [703]
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Authors: del Zoppo, G. J.
Venue: Neuroscience
Publisher: Elsevier BV
Published: 2009-02
Volume: 158
Issue: 3
Pages: 972-982
ISSN: 0306-4522 (ISSN-L)
DOI: 10.1016/j.neuroscience.2008.08.028
PMC: PMC2665879
OpenAlex: W2126479164
Cited by: 243
References: 86
Citations by year: 2026: 6 · 2025: 4 · 2024: 9 · 2023: 11 · 2022: 9 · 2021: 19 · 2020: 11 · 2019: 22 · 2018: 11 · 2017: 21 · 2016: 17 · 2015: 16 · 2014: 17 · 2013: 14 · 2012: 20
FWCI: 1.00
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Neurological Disorders and Stroke (R01NS026945, R01NS053716, R01NS038710, R37NS038710)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
Keywords: neurovascular unit, focal cerebral ischemia, neuroinflammation, microvessels, neurons, glial cells, proteolytic enzymes, inflammatory mediators, ischemic response
MeSH terms: Animals, Basement Membrane, Blood-Brain Barrier, Capillaries, Cell Communication, Brain Ischemia, Encephalitis, Humans, Microcirculation, Neuroglia, Neurons, Endothelial Cells

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Inflammation and the neurovascular unit in the setting of focal cerebral ischemia

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