scholarly journals Lipocalin-2 Deficiency Attenuates Neuroinflammation and Brain Injury after Transient Middle Cerebral Artery Occlusion in Mice

2014 ◽  
Vol 34 (8) ◽  
pp. 1306-1314 ◽  
Author(s):  
Myungwon Jin ◽  
Jong-Heon Kim ◽  
Eunha Jang ◽  
Young Mi Lee ◽  
Hyung Soo Han ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Lipocalin 2 ◽  
Ischemic Brain ◽  
Cerebral Artery Occlusion

Lipocalin-2 (LCN2) is a secreted protein of the lipocalin family, but little is known about the expression or the role of LCN2 in the central nervous system. Here, we investigated the role of LCN2 in ischemic stroke using a rodent model of transient cerebral ischemia. Lipocalin-2 expression was highly induced in the ischemic brain and peaked at 24 hours after reperfusion. After transient middle cerebral artery occlusion, LCN2 was predominantly expressed in astrocytes and endothelial cells, whereas its receptor (24p3R) was mainly detected in neurons, astrocytes, and endothelial cells. Brain infarct volumes, neurologic scores, blood–brain barrier (BBB) permeabilities, glial activation, and inflammatory mediator expression were significantly lower in LCN2-defkient mice than in wild-type animals. Lipocalin-2 deficiency also attenuated glial neurotoxicity in astrocyte/neuron cocultures after oxygen-glucose deprivation. Our results indicate LCN2 has a critical role in brain injury after ischemia/reperfusion, and that LCN2 may contribute to neuronal cell death in the ischemic brain by promoting neurotoxic glial activation, neuroinflammation, and BBB disruption.

scholarly journals Silencing of lncRNA XLOC_035088 Protects Middle Cerebral Artery Occlusion-Induced Ischemic Stroke by Notch1 Signaling

2020 ◽  
Vol 80 (1) ◽  
pp. 60-70
Author(s):  
Miao Chen ◽  
Feng Wang ◽  
Hairong Wang
Keyword(s):  
Ischemic Stroke ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Hippocampal Neurons ◽  
Artery Occlusion ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Cerebral Artery Occlusion

Abstract Ischemic stroke represents one of the leading causes of mortality worldwide and especially in developing countries. It is crucial for finding effective therapeutic targets that protect the brain against ischemic injury. Long noncoding RNAs (lncRNAs) have emerged as major regulators of neurological diseases, and clarifying their roles in cerebral ischemic injury may provide novel targets for the treatment of ischemic stroke. We aimed to investigate the role of lncRNA-XLOC_035088 in middle cerebral artery occlusion (MCAO)-induced rat brain injury and oxygen-glucose deprivation (OGD)-reperfusion treated hippocampal neurons. In our findings, we found that XLOC_035088 expression was significantly upregulated in OGD-reperfusion treated hippocampal neurons and in different brain regions of MCAO-treated rats. XLOC_035088 silencing protected against MCAO-induced ischemic brain injury in vivo and OGD-induced hippocampal neuronal apoptosis in vitro. Intrahippocampal silencing of XLOC_035088 significantly decreased brain XLOC_035088 expression, reduced brain infarct size, and improved neurological function through inhibiting NOTCH1 following derepression of presenilin 2 (PSEN2). Taken together, this study provides evidence that the lncRNA XLOC_035088/PSEN2/Notch1 axis is involved in the pathogenesis of ischemic brain injury, and presents a promising therapeutic route for ischemic stroke.

Role of cell adhesion molecules in brain injury after transient middle cerebral artery occlusion in the rat

1994 ◽  
Vol 656 (2) ◽  
pp. 344-352 ◽  
Author(s):  
Yoshiyuki Matsuo ◽  
Hiroshi Onodera ◽  
Yusei Shiga ◽  
Hidetaka Shozuhara ◽  
Mitsuyoshi Ninomiya ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Adhesion Molecules ◽  
Cerebral Artery ◽  
Cell Adhesion Molecules ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion
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