MicroRNA-150 contributes to ischemic stroke through its effect on cerebral cortical neuron survival and function by inhibiting ERK1/2 axis via Mal

2018 ◽  
Vol 234 (2) ◽  
pp. 1477-1490 ◽  
Author(s):  
Hui Lv ◽  
Jie Li ◽  
Yu-Qin Che
Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Michelle C Johansen ◽  
Henrique Doria De Vasconcellos ◽  
Rebecca Gottesman

Background: Accruing evidence suggests that changes in cardiac structure and function, irrespective of tachyarrhythmia, are responsible for thrombus formation. Although transthoracic echocardiogram (TTE) is frequently used for cardiovascular evaluation in ischemic stroke patients (IS), many cardiac features that could clarify stroke subtype are poorly characterized without optimal evaluation of the left atrium (LA). 2D speckle tracking echocardiography (STE) allows an accurate, reproducible, and detailed assessment of the LA cycle. Methods: IS with clinically indicated TTE provided consent. LA STE was quantified using a post processing wall motion tracking software per standard definitions. Strain/strain rate (Sr) curves for the 3 components of the LA cycle: 1) Reservoir (Global longitudinal Sr (Srmax)) 2) Conductive (Early LA Sr (Sre)) and 3) Contractile (Late LA Sr (Sra)) were evaluated. The association of embolic-appearing stroke (cardioembolic or cryptogenic; ES) with LA STE features (independent variables) was tested using logistic regression (OR (95%CI)) adjusted for covariates. Results: Participants (N=136) were 53-70yo, 57% female and 59% black. Incremental increases in Sra (worse LA contraction) were associated with >2 times greater odds of ES (2.47 (1.29-4.72)) and improvement in Smax (LA reservoir) was associated with decreased odds of ES when adjusting for demographics (0.98 (0.96-0.99)), but not in a fully adjusted model. Improvement in the corresponding emptying fractions was significantly associated with decreased odds of ES (aEF 0.93 (0.98-0.97) tEF 0.96 ( 0.93-0.99)). Conclusions: In this study the odds of ES was higher in those with worse LA contraction and decreased with improvement in LA reservoir with corresponding decreased odds of ES with improvement in emptying fractions. LA STE is an underutilized technology and may represent a promising tool for characterization of LA performance in patients with otherwise unexplained ES.


PM&R ◽  
2020 ◽  
Author(s):  
Chen Lin ◽  
Jungwha Lee ◽  
Christopher P. Hurt ◽  
Ronald M. Lazar ◽  
Yurany A. Arevalo ◽  
...  

2020 ◽  
Vol 41 (8) ◽  
pp. 2215-2223 ◽  
Author(s):  
AnNa Ying ◽  
YaNi Cheng ◽  
YanYan Lin ◽  
JunRu Yu ◽  
XiaoYun Wu ◽  
...  
Keyword(s):  

Neuron ◽  
2016 ◽  
Vol 90 (6) ◽  
pp. 1215-1229 ◽  
Author(s):  
Yosuke Tanaka ◽  
Shinsuke Niwa ◽  
Ming Dong ◽  
Atena Farkhondeh ◽  
Li Wang ◽  
...  

1998 ◽  
Vol 813 (2) ◽  
pp. 313-322 ◽  
Author(s):  
Günter U Höglinger ◽  
Jürgen Sautter ◽  
Morten Meyer ◽  
Christian Spenger ◽  
Rolf W Seiler ◽  
...  

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Zhongjun Chen ◽  
Tieping Fan ◽  
Xusheng Zhao ◽  
Zhichen Zhang

Abstract Objectives Studies have widely explored in the filed of ischemic stroke (IS) with their focus on transcription factors. However, few studies have pivoted on sex determining region Y-box 2 (SOX2) in IS. Thus, this study is launched to figure out the mechanisms of SOX2 in IS. Methods Rat middle cerebral artery occlusion (MCAO) was established as a stroke model. MCAO rats were injected with depleted SOX2 or long non-coding RNA plasmacytoma variant translocation 1 (PVT1) to explore their roles in neurological deficits, cerebral water content, neuron survival, apoptosis and oxidative stress. The relationship among SOX2, PVT1, microRNA (miR)-24-3p and signal transducer and activator of transcription 3 (STAT3) was verified by a series of experiments. Results SOX2, PVT1 and STAT3 were highly expressed while miR-24-3p was poorly expressed in cerebral cortex tissues of MCAO rats. Depleted SOX2 or PVT1 alleviated brain injury in MCAO rats as reflected by neuronal apoptosis and oxidative stress restriction, brain water content reduction, and neurological deficit and neuron survival improvements. Overexpression of PVT1 functioned oppositely. Restored miR-24-3p abolished PVT1 overexpression-induced brain injury in MCAO rats. SOX2 directly promoted PVT1 expression and further increased STAT3 by sponging miR-24-3p. Conclusion This study presents that depleting SOX2 improves IS via PVT1/miR-24-3p/STAT3 axis which may broaden our knowledge about the mechanisms of SOX2/PVT1/miR-24-3p/STAT3 axis and provide a reference of therapy for IS.


2020 ◽  
Vol 21 (10) ◽  
pp. 3618 ◽  
Author(s):  
Anna Kloska ◽  
Marcelina Malinowska ◽  
Magdalena Gabig-Cimińska ◽  
Joanna Jakóbkiewicz-Banecka

Stroke is a severe neurological disorder in humans that results from an interruption of the blood supply to the brain. Worldwide, stoke affects over 100 million people each year and is the second largest contributor to disability. Dyslipidemia is a modifiable risk factor for stroke that is associated with an increased risk of the disease. Traditional and non-traditional lipid measures are proposed as biomarkers for the better detection of subclinical disease. In the central nervous system, lipids and lipid mediators are essential to sustain the normal brain tissue structure and function. Pathways leading to post-stroke brain deterioration include the metabolism of polyunsaturated fatty acids. A variety of lipid mediators are generated from fatty acids and these molecules may have either neuroprotective or neurodegenerative effects on the post-stroke brain tissue; therefore, they largely contribute to the outcome and recovery from stroke. In this review, we provide an overview of serum lipids associated with the risk of ischemic stroke. We also discuss the role of lipid mediators, with particular emphasis on eicosanoids, in the pathology of ischemic stroke. Finally, we summarize the latest research on potential targets in lipid metabolic pathways for ischemic stroke treatment and on the development of new stroke risk biomarkers for use in clinical practice.


2021 ◽  
Vol 15 ◽  
Author(s):  
Xin-Ya Shen ◽  
Zhen-Kun Gao ◽  
Yu Han ◽  
Mei Yuan ◽  
Yi-Sha Guo ◽  
...  

Ischemic stroke refers to the disorder of blood supply of local brain tissue caused by various reasons. It has high morbidity and mortality worldwide. Astrocytes are the most abundant glial cells in the central nervous system (CNS). They are responsible for the homeostasis, nutrition, and protection of the CNS and play an essential role in many nervous system diseases’ physiological and pathological processes. After stroke injury, astrocytes are activated and play a protective role through the heterogeneous and gradual changes of their gene expression, morphology, proliferation, and function, that is, reactive astrocytes. However, the position of reactive astrocytes has always been a controversial topic. Many studies have shown that reactive astrocytes are a double-edged sword with both beneficial and harmful effects. It is worth noting that their different spatial and temporal expression determines astrocytes’ various functions. Here, we comprehensively review the different roles and mechanisms of astrocytes after ischemic stroke. In addition, the intracellular mechanism of astrocyte activation has also been involved. More importantly, due to the complex cascade reaction and action mechanism after ischemic stroke, the role of astrocytes is still difficult to define. Still, there is no doubt that astrocytes are one of the critical factors mediating the deterioration or improvement of ischemic stroke.


Sign in / Sign up

Export Citation Format

Share Document