scholarly journals The evolving role of neuro-immune interaction in brain repair after cerebral ischemic stroke

2018 ◽  
Vol 24 (12) ◽  
pp. 1100-1114 ◽  
Author(s):  
Xin Wang ◽  
Wei Xuan ◽  
Zi-Yu Zhu ◽  
Yan Li ◽  
Hao Zhu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Brain Repair ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

scholarly journals Role of angiogenesis in patients with cerebral ischemic stroke.

Stroke ◽  
1994 ◽  
Vol 25 (9) ◽  
pp. 1794-1798 ◽  
Author(s):  
J Krupinski ◽  
J Kaluza ◽  
P Kumar ◽  
S Kumar ◽  
J M Wang
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

scholarly journals Overexpression of MicroRNA-145 Ameliorates Astrocyte Injury by Targeting Aquaporin 4 in Cerebral Ischemic Stroke

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Lifang Zheng ◽  
Wei Cheng ◽  
Xijia Wang ◽  
Zhigang Yang ◽  
Xiangling Zhou ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Ischemic Injury ◽  
Glucose Deprivation ◽  
Expression Levels ◽  
Cultured Astrocytes ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Induced Apoptosis ◽  
Global Population

Cerebral ischemic stroke, which affects the global population, is a major disease with high incidence, mortality, and disability. Accumulating evidence has indicated that abnormal microRNA (miRNA) expression plays essential roles in the pathologies of ischemic stroke. Yet, the underlying regulatory mechanism of miRNAs in cerebral ischemic stroke remains unclear. We investigated the role of miR-145 in cerebral ischemic stroke and its potential mechanism in a model using primary cultured astrocytes. We detected the expression levels of miR-145 and its target gene AQP4 and assessed the role of miR-145 in cell death and apoptosis caused by oxygen-glucose deprivation (OGD). Bioinformatics analysis was used to explore the targets of miR-145. miR-145 expression levels were significantly decreased in primary astrocytes subjected to OGD. miR-145 overexpression promoted astrocyte health and inhibited OGD-induced apoptosis. AQP4 was a direct target of miR-145, and miR-145 suppressed AQP4 expression. Moreover, AQP4 enhanced astrocyte injury in ischemic stroke, and AQP4 knockdown diminished the miR-145-mediated protective effect on ischemic injury. Taken together, our results show that miR-145 plays an important role in protecting astrocytes from ischemic injury by downregulating AQP4 expression. These findings may highlight a novel therapeutic target in cerebral ischemic stroke.

The Role of Exogenous Neural Stem Cells Transplantation in Cerebral Ischemic Stroke

2014 ◽  
Vol 10 (11) ◽  
pp. 3219-3230 ◽  
Author(s):  
Lukui Chen ◽  
Rong Qiu ◽  
Lushen Li ◽  
Dan He ◽  
Haiqin Lv ◽  
...  
Keyword(s):  
Stem Cells ◽  
Ischemic Stroke ◽  
Neural Stem Cells ◽  
Stem Cells Transplantation ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

scholarly journals The role of KATP channels in cerebral ischemic stroke and diabetes

2018 ◽  
Vol 39 (5) ◽  
pp. 683-694 ◽  
Author(s):  
Vivian Szeto ◽  
Nai-hong Chen ◽  
Hong-shuo Sun ◽  
Zhong-ping Feng
Keyword(s):  
Ischemic Stroke ◽  
Katp Channels ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Major Complication ◽  
Lactic Dehydrogenase ◽  
Dependent Manner ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Myd88 Signaling ◽  
Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

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