Microglial activation and brain injury after intracerebral hemorrhage

2009 ◽  
pp. 59-65 ◽  
Author(s):  
J. Wu ◽  
S. Yang ◽  
G. Xi ◽  
S. Song ◽  
G. Fu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Microglial Activation

scholarly journals Gap Junctions and Hemichannels Composed of Connexins and Pannexins Mediate the Secondary Brain Injury following Intracerebral Hemorrhage

Biology ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 27
Author(s):  
Yan Zhang ◽  
Suliman Khan ◽  
Yang Liu ◽  
Rabeea Siddique ◽  
Ruiyi Zhang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Gap Junctions ◽  
Reactive Nitrogen Species ◽  
Microglial Activation ◽  
Functional Independence ◽  
Secondary Brain Injury ◽  
Mortality And Morbidity ◽  
Cytokines And Chemokines ◽  
Phenotypic Transformation

Intracerebral hemorrhage (ICH) is a devastating disease with high mortality and morbidity; the mortality rate ranges from 40% at 1 month to 54% at 1 year; only 12%−39% achieve good outcomes and functional independence. ICH affects nearly 2 million patients worldwide annually. In ICH development, the blood leakage from ruptured vessels generates sequelae of secondary brain injury (SBI). This mechanism involves activated astrocytes and microglia, generation of reactive oxygen species (ROS), the release of reactive nitrogen species (RNS), and disrupted blood brain barrier (BBB). In addition, inflammatory cytokines and chemokines, heme compounds, and products of hematoma are accumulated in the extracellular spaces, thereby resulting in the death of brain cells. Recent evidence indicates that connexins regulate microglial activation and their phenotypic transformation. Moreover, communications between neurons and glia via gap junctions have crucial roles in neuroinflammation and cell death. A growing body of evidence suggests that, in addition to gap junctions, hemichannels (composed of connexins and pannexins) play a key role in ICH pathogenesis. However, the precise connection between connexin and pannexin channels and ICH remains to be resolved. This review discusses the pathological roles of gap junctions and hemichannels in SBI following ICH, with the intent of discovering effective therapeutic options of strategies to treat ICH.

Microglial Activation as a Compelling Target for Treating Acute Traumatic Brain Injury

2015 ◽  
Vol 22 (6) ◽  
pp. 759-770 ◽  
Author(s):  
Chung-Ching Chio ◽  
Mao-Tsun Lin ◽  
Ching-Ping Chang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Microglial Activation ◽  
Acute Traumatic Brain Injury

The role of complement in brain injury following intracerebral hemorrhage: A review

2021 ◽  
pp. 113654
Author(s):  
Katherine Holste ◽  
Fan Xia ◽  
Hugh J.L. Garton ◽  
Shu Wan ◽  
Ya Hua ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage

Ginsenoside Rg2 Ameliorates Brain Injury After Intracerebral Hemorrhage in a Rat Model of Preeclampsia

2021 ◽  
Author(s):  
Liying Cai ◽  
Feifei Hu ◽  
Wenwen Fu ◽  
Xiaofeng Yu ◽  
Weijie Zhong ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Rat Model

scholarly journals Biglycan regulates neuroinflammation by promoting M1 microglial activation in early brain injury after experimental subarachnoid hemorrhage

2019 ◽  
Vol 152 (3) ◽  
pp. 368-380 ◽  
Author(s):  
Yuke Xie ◽  
Jianhua Peng ◽  
Jinwei Pang ◽  
Kecheng Guo ◽  
Lifang Zhang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Microglial Activation ◽  
Early Brain Injury ◽  
Experimental Subarachnoid Hemorrhage

Abstract W P222: Activated Microglia Contribute to Neurovascular Integrity and Limit Brain Injury After Acute Neonatal Focal Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
David Fernández-López ◽  
Joel Faustino ◽  
Alexander Klibanov ◽  
Nikita Derugin ◽  
katerina Akassoglou ◽  
...  
Keyword(s):  
Brain Injury ◽  
Microglial Activation ◽  
Injury Severity ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Microglial Cells ◽  
Vascular Density ◽  
Relative Role ◽  
Morphological Transformation ◽  
Activated Microglia

It has been recently shown that microglial cells, which for a long time were considered purely injurious in the context of cerebral ischemia, can also exert beneficial effects following stroke in both adults and neonates1,2. Lack of tools to reliably distinguish resident microglia from infiltrated peripheral monocytes has been a major obstacle on the way to understand the relative role of these subpopulations of cells of the monocyte lineage in the pathophysiology of stroke. We subjected postnatal day 10 (P10) transgenic Cx3cr1GFP/-CCr2RFP/- mice, in which resident microglia (Cx3cr1GFP) and infiltrating monocytes (CCr2RFP) can be distinctively identified, to a transient 3 hour middle cerebral artery occlusion MCAO, a model that we recently developed3. Microglial cells were left unperturbed or were selectively depleted before MCAO by intracortical injection of clodronate-encapsulated liposomes. Depletion of microglia exacerbated injury and significantly increased infarct volume (75.9% Vs. 56.3%, p<0.01). Furthermore, compared to mice with unperturbed microglia, depletion of microglia significantly increased the number of hemorrhages in injured regions, adversely affected vascular density and decreased the number of both adherent and infiltrated monocytes. The extent of RFP+ monocyte adhesion to vessels and infiltration in the brain parenchyma was highly variable among individual mice and did not correlate with brain infarct, whereas a significant correlation between the overall extent of microglial activation (measured by morphological transformation) and the number of infiltrated monocytes was observed. The deleterious effect of microglial depletion on vascular integrity and function and on brain injury indicates that activated microglia act as a buffering component that limits vascular degeneration and injury severity after neonatal stroke. Our data also suggest a direct and dynamic relationship between microglial activation and monocyte recruitment into acutely reperfused neonatal brain. Support: NS55915 (ZV), NS76726 (ZV), NS080015 (ZS, KA), AHA POST10980003 (DFL). 1. Faustino J et al. J Neurosci. 2011. 2. Lalancette-Hebert M et al. J Neurosci. 2007. 3. Woo MS et al. Annals of Neurology. 2012.

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