scholarly journals Critical role of neuronal pentraxin 1 in mitochondria-mediated hypoxic–ischemic neuronal injury

2013 ◽  
Vol 50 ◽  
pp. 59-68 ◽  
Author(s):  
Md Al Rahim ◽  
Shabarish Thatipamula ◽  
Mir Ahamed Hossain
Keyword(s):  
Critical Role ◽  
Neuronal Injury ◽  
Neuronal Pentraxin ◽  
Ischemic Neuronal Injury

scholarly journals Critical Role of Calpain I in Mitochondrial Release of Apoptosis-Inducing Factor in Ischemic Neuronal Injury

2007 ◽  
Vol 27 (35) ◽  
pp. 9278-9293 ◽  
Author(s):  
G. Cao ◽  
J. Xing ◽  
X. Xiao ◽  
A. K. F. Liou ◽  
Y. Gao ◽  
...  
Keyword(s):  
Critical Role ◽  
Neuronal Injury ◽  
Apoptosis Inducing Factor ◽  
Ischemic Neuronal Injury

scholarly journals The Role of SUMO-Conjugating Enzyme Ubc9 in the Neuroprotection of Isoflurane Preconditioning Against Ischemic Neuronal Injury

2014 ◽  
Vol 51 (3) ◽  
pp. 1221-1231 ◽  
Author(s):  
Li Tong ◽  
Zhixin Wu ◽  
Mingzi Ran ◽  
Yu Chen ◽  
Lujia Yang ◽  
...  
Keyword(s):  
Neuronal Injury ◽  
Ischemic Neuronal Injury ◽  
Conjugating Enzyme

scholarly journals Upregulation of Extracellular Vesicles-Encapsulated miR-132 Released From Mesenchymal Stem Cells Attenuates Ischemic Neuronal Injury by Inhibiting Smad2/c-jun Pathway via Acvr2b Suppression

2021 ◽  
Vol 8 ◽  
Author(s):  
Bin Feng ◽  
Lei Meng ◽  
Liming Luan ◽  
Zhihao Fang ◽  
Peng Zhao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Extracellular Vesicles ◽  
Neuronal Cell ◽  
Neuronal Injury ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Gene Assay ◽  
Ischemic Neuronal Injury

Ischemic cerebrovascular disease is a significant and common public health issue worldwide. The emerging roles of mesenchymal stem cells (MSCs)-derived extracellular vesicles (EVs) in ischemic neuronal injury continue to be investigated. The current study aimed to investigate the role of EV-derived miR-132 from MSCs in ischemic neuronal injury. EVs were initially isolated from bone MSCs (BMSCs) and subsequently evaluated. A middle cerebral artery occlusion (MCAO) mouse model was constructed with the neurological function evaluated through a series of neurological scores, a pole test, and a foot fault test. Histopathological changes, neuron viability, and apoptosis, as well as cerebral infarction, were detected by hematoxylin and eosin (HE) staining and 2,3,5-triphenyltetrazolium hydrochloride (TTC) staining. The targeting relationship between microRNA (miR)-132 and Activin receptor type IIB (Acvr2b) was further confirmed based on dual-luciferase reporter gene assay results. Loss- and gain-of-function assays were conducted to elucidate the role of miR-132, EV-derived miR-132, Acvr2b, and Smad2 in oxygen-glucose deprivation (OGD)-treated neurons, and in mice models. Neuronal cell viability and apoptosis were evaluated via Cell Counting kit-8 (CCK-8) and flow cytometry. Our results indicated that Acvr2b was highly expressed, while miR-132 was poorly expressed in the MCAO mice and OGD-treated neurons. Acvr2b silencing or upregulation of miR-132 led to an elevation in neuronal activity, decreased neuronal apoptosis, reduced expression of Bax, and cleaved-caspase 3, as well as increased Bcl-2 expression. Acvr2b expression was targeted and inhibited by miR-132. EV-derived Acvr2b promoted activation of phosphorylated-Smad2 (p-Smad2)/c-jun signaling pathway, ultimately inducing neuronal injury. Our study provides evidence demonstrating that the overexpression of c-jun inhibits the protective role of MSCs-derived EV-miR-132 in neuronal injury. Upregulation of EV-derived miR-132 released from MSCs attenuates ischemic neuronal injury by inhibiting Smad2/c-jun pathways via the suppression of Acvr2b.

scholarly journals The Role of Parl and HtrA2 in Striatal Neuronal Injury After Transient Global Cerebral Ischemia

2013 ◽  
Vol 33 (11) ◽  
pp. 1658-1665 ◽  
Author(s):  
Hideyuki Yoshioka ◽  
Masataka Katsu ◽  
Hiroyuki Sakata ◽  
Nobuya Okami ◽  
Takuma Wakai ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Small Interfering Rna ◽  
Neuronal Injury ◽  
Global Cerebral Ischemia ◽  
Inhibitor Of Apoptosis ◽  
Transient Global Cerebral Ischemia ◽  
Apoptosis Protein ◽  
Interfering Rna ◽  
Ischemic Neuronal Injury

The presenilin-associated rhomboid-like (PARL) protein and high temperature requirement factor A2 (HtrA2) are key regulators of mitochondrial integrity and play pivotal roles in apoptosis. However, their roles after cerebral ischemia have not been thoroughly elucidated. To clarify these roles, mice were subjected to transient global cerebral ischemia, and striatal neuronal injury was assessed. Western blot and coimmunoprecipitation analyses revealed that PARL and processed HtrA2 localized to mitochondria, and that PARL was bound to HtrA2 in sham animals. Expression of PARL and processed HtrA2 in mitochondria significantly decreased 6 to 72 hours after ischemia, and the binding of PARL to HtrA2 disappeared after ischemia. In contrast, expression of processed HtrA2 increased 24 hours after ischemia in the cytosol, where HtrA2 was bound to X chromosome-linked inhibitor-of-apoptosis protein (XIAP). Administration of PARL small interfering RNA inhibited HtrA2 processing and worsened ischemic neuronal injury. Our results show that downregulation of PARL after ischemia is a key step in ischemic neuronal injury, and that it decreases HtrA2 processing and increases neuronal vulnerability. In addition, processed HtrA2 released into the cytosol after ischemia contributes to neuronal injury via inhibition of XIAP.

scholarly journals Ischemic Neuronal Injury is Ameliorated by Astrocyte Activation

1998 ◽  
Vol 25 (2) ◽  
pp. 102-107 ◽  
Author(s):  
Deon F. Louw ◽  
Tetsuy Masada ◽  
Garnette R. Sutherland
Keyword(s):  
Ethidium Bromide ◽  
Neuronal Injury ◽  
Contralateral Side ◽  
Forebrain Ischemia ◽  
Astrocyte Activation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Sector ◽  
Ischemic Neuronal Injury

ABSTRACT:Background:The motivation of this study was to more precisely define the in vivo role of astrocytes in forebrain ischemia. Controversy exists in the literature as to whether they protect or injure neurons in this setting.Methods:Astrocytes in the rat hippocampus were disabled with stereotactic administration of a gliotoxin, ethidium bromide, 3 days prior to induction of forebrain ischemia. The extent of neuronal injury in this group was compared to a control category receiving intrahippocampal saline only.Results:Saline-injected animals demonstrated decreased hippocampal CA1 sector injury, and increased gliosis on the side of the injection compared to the contralateral side (P < 0.01) or ethidium bromide-treated animals (P < 0.05).Conclusion:The results suggest that activated astrocytes are protective to neurons subjected to an ischemic insult. This may result from their ability to elaborate neurotrophic factors, buffer potassium and metabolize a variety of neurotransmitters.

Role of Cav2.3 (α1E) Ca2+ channel in ischemic neuronal injury

Neuroreport ◽  
2002 ◽  
Vol 13 (2) ◽  
pp. 261-265 ◽  
Author(s):  
Hideyuki Toriyama ◽  
Ling Wang ◽  
Hironao Saegusa ◽  
Shuqin Zong ◽  
Makoto Osanai ◽  
...  
Keyword(s):  
Neuronal Injury ◽  
Ischemic Neuronal Injury
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