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Cited by 359Barrier Structure and Function StudiesNeuroinflammation and Neurodegeneration MechanismsAcute Ischemic Stroke Management

Microglia Potentiate Damage to Blood–Brain Barrier Constituents: Improvement by Minocycline In Vivo and In Vitro

Yenari, Midori A., Xu, Lijun, Tang, Xian Nan, Qiao, Yanli, Giffard, Rona G.·2006·Stroke
DOI 10.1161/01.str.0000206281.77178.ac
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Abstract

BACKGROUND: Blood-brain barrier (BBB) disruption after stroke can worsen ischemic injury by increasing edema and causing hemorrhage. We determined the effect of microglia on the BBB and its primary constituents, endothelial cells (ECs) and astrocytes, after ischemia using in vivo and in vitro models. METHODS AND RESULTS: Primary astrocytes, ECs, or cocultures were prepared with or without added microglia. Primary ECs were more resistant to oxygen-glucose deprivation/reperfusion than astrocytes. ECs plus astrocytes showed intermediate vulnerability. Microglia added to cocultures nearly doubled cell death. This increase was prevented by minocycline and apocynin. In vivo, minocycline reduced infarct volume and neurological deficits and markedly reduced BBB disruption and hemorrhage in mice after experimental stroke. CONCLUSIONS: Inhibition of microglial activation may protect the brain after ischemic stroke by improving BBB viability and integrity. Microglial inhibitors may prove to be an important treatment adjunct to fibrinolysis.

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  • Inhibiting microglial activation may limit BBB disruption and reduce vasogenic edema in ischemic stroke, reducing ischemic tissue volume and neuronal deficits, and preventing hemorrhagic transformation.

    “Inhibiting microglial activation may limit BBB disruption and reduce vasogenic edema in the context of ischemic stroke, reducing the volume of ischemic tissue and neuronal deficits, as well as preventing hemorrhagic transformation (Tikka et al., 2001; Yenari et al., 2006).”

    From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Yenari et al., 2006

  • Inhibition of microglial activation by minocycline favors differentiation of oligodendrocyte precursors and immature oligodendrocytes, which are responsible for remyelination of neurons, an important event for improvement of MS condition.

    “The inhibition of microglial activation by minocycline favors the differentiation of oligodendrocyte precursors and immature oligodendrocytes. These cells are responsible for remyelination of neurons, an important event for improvement of MS condition (Li et al., 2005; Yenari et al., 2006; Defaux et al., 2011; Miron et al., 2013).”

    From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Yenari et al., 2006

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Authors
Yenari, M. A., Xu, L., Tang, X. N., Qiao, Y., & Giffard, R. G.
Affiliations
San Francisco VA Medical Center (US)
ORCID
Venue
Stroke
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2006-04
Volume
37
Issue
4
Pages
1087-1093
ISSN
  • 0039-2499 (ISSN-L)
  • 1524-4628
DOI
10.1161/01.str.0000206281.77178.ac
OpenAlex
W1973393911
Cited by
359
References
41
Citations by year
2026: 10 · 2025: 12 · 2024: 22 · 2023: 13 · 2022: 20 · 2021: 18 · 2020: 14 · 2019: 19 · 2018: 22 · 2017: 14 · 2016: 11 · 2015: 26 · 2014: 27 · 2013: 18 · 2012: 23
FWCI
11.17
Type
journal article
Language
en
Open access
closed
Locations
  • Stroke (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of General Medical Sciences (R01GM049831, R01 GM 49831)
  • National Institute of Neurological Disorders and Stroke (P50NS014543, R01 NS 40516, P01 NS 37520, P01NS037520, R01NS040516, P50NS14543)
Topics
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
Keywords
microglia, blood-brain barrier disruption, ischemic stroke, endothelial cells, astrocytes, minocycline, apocynin, microglial activation, oxygen-glucose deprivation/reoxygenation, hemorrhagic transformation, infarct size, neurological deficit
MeSH terms
Acetophenones, Animals, Hypoxia, Antioxidants, Astrocytes, Blood-Brain Barrier, Brain, Cells, Cultured, Cerebral Hemorrhage, Cerebral Infarction, Brain Ischemia, Glucose, Hydrogen Peroxide, Male, Mice, Inbred C57BL, Minocycline, Nervous System Diseases, Superoxides, Tumor Necrosis Factor-alpha, Cell Death, Microglia, Coculture Techniques, Endothelial Cells, Mice

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