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Molecular Signaling in Stroke
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Molecular Signaling in Stroke

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 17846

Special Issue Editors

Dr. Saif Ahmad

E-Mail Website
Guest Editor
Department of Neurosurgery and Neurobiology, Barrow Neurological Institute, SJHMC, Dignity Health, Phoenix, AZ, USA
Interests: neurovascular dysfunction; stroke; VCID; TBI; Traumatic Optic Neuropathy (TON); diabetes; neurodegenerative disorders
Special Issues, Collections and Topics in MDPI journals
Dr. Naseem Akhter

E-Mail Website
Guest Editor
Department of Laboratory Medicine, Faculty of Applied Medical Sciences, Albaha University, Albaha 65431, Saudi Arabia
Interests: biochemistry; pharmacology; genetics

Special Issue Information

Dear Colleagues,

A Special Issue on the pertinent topic “Molecular Signaling in Stroke" is being prepared for the journal IJMS. Despite the large amount of fundamental research focused on ischemic and hemorrhagic stroke, much remains to be elucidated pertaining to molecular mechanisms central to stroke; for example, the role of amyloid-beta protein in iatrogenic amyloid-beta cerebral amyloid angiopathy (iCAA) in stroke. MicroRNAs influence the onset, pathophysiology and outcome of stroke. Several animal and human studies have elucidated the mechanism of miRNAs expression in brain and blood after ischemic or hemorrhagic injury. Recent research has also led to the identification of a few diagnostic and prognostic markers along with neuroprotective drug targets. Fundamental miRNA research in stroke has a potential to lead to important discoveries and, in turn, significant therapeutic applications. Some rare inherited disorders, such as cerebral autosomal dominant arteriopathy, are associated with stroke incidence. Recently, complement proteins (C3aR and C1q) have shown the important role in the pathophysiology of stroke.  The identification of the additional genes will lead to a greater level of knowledge about stroke and the discovery of new treatments. Original manuscripts and reviews dealing with the mechanisms involved in hypercoagulability, endothelial injury, disseminated intravascular coagulation, necrotizing encephalopathy, vasculitis, cardiomyopathy, micro vascular thrombosis, deep venous thrombosis and systematic hypoxia associated with stroke are warmly welcome.

Dr. Saif Ahmad
Dr. Naseem Akhter
Guest Editors

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Published Papers (6 papers)

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Editorial

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3 pages, 190 KiB  
Editorial
Molecular Signaling in Stroke
by Naseem Akhter and Saif Ahmad
Int. J. Mol. Sci. 2023, 24(6), 5975; https://doi.org/10.3390/ijms24065975 - 22 Mar 2023
Viewed by 1516
Abstract
We have reached the end of the Special Issue on Molecular Signaling in Stroke in IJMS [...] Full article
(This article belongs to the Special Issue Molecular Signaling in Stroke)

Research

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16 pages, 2368 KiB  
Article
Comparative Use of Contralateral and Sham-Operated Controls Reveals Traces of a Bilateral Genetic Response in the Rat Brain after Focal Stroke
by Ivan B. Filippenkov, Julia A. Remizova, Alina E. Denisova, Vasily V. Stavchansky, Ksenia D. Golovina, Leonid V. Gubsky, Svetlana A. Limborska and Lyudmila V. Dergunova
Int. J. Mol. Sci. 2022, 23(13), 7308; https://doi.org/10.3390/ijms23137308 - 30 Jun 2022
Cited by 5 | Viewed by 2213
Abstract
Ischemic stroke is a multifactorial disease with a complex etiology and global consequences. Model animals are widely used in stroke studies. Various controls, either brain samples from sham-operated (SO) animals or symmetrically located brain samples from the opposite (contralateral) hemisphere (CH), are often [...] Read more.
Ischemic stroke is a multifactorial disease with a complex etiology and global consequences. Model animals are widely used in stroke studies. Various controls, either brain samples from sham-operated (SO) animals or symmetrically located brain samples from the opposite (contralateral) hemisphere (CH), are often used to analyze the processes in the damaged (ipsilateral) hemisphere (IH) after focal stroke. However, previously, it was shown that focal ischemia can lead to metabolic and transcriptomic changes not only in the IH but also in the CH. Here, using a transient middle cerebral artery occlusion (tMCAO) model and genome-wide RNA sequencing, we identified 1941 overlapping differentially expressed genes (DEGs) with a cutoff value >1.5 and Padj < 0.05 that reflected the general transcriptome response of IH subcortical cells at 24 h after tMCAO using both SO and CH controls. Concomitantly, 861 genes were differentially expressed in IH vs. SO, whereas they were not vs. the CH control. Furthermore, they were associated with apoptosis, the cell cycle, and neurotransmitter responses. In turn, we identified 221 DEGs in IH vs. CH, which were non-DEGs vs. the SO control. Moreover, they were predominantly associated with immune-related response. We believe that both sets of non-overlapping genes recorded transcriptome changes in IH cells associated with transhemispheric differences after focal cerebral ischemia. Thus, the specific response of the CH transcriptome should be considered when using it as a control in studies of target brain regions in diseases that induce a global bilateral genetic response, such as stroke. Full article
(This article belongs to the Special Issue Molecular Signaling in Stroke)
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16 pages, 1670 KiB  
Article
Enhanced Ca2+ Entry Sustains the Activation of Akt in Glucose Deprived SH-SY5Y Cells
by Maria Kourti, Danai Liaropoulou, Maria Paschou, Ioanna Giagklisi, Maria Paschalidi, Evangelia Petani and Panagiota Papazafiri
Int. J. Mol. Sci. 2022, 23(3), 1386; https://doi.org/10.3390/ijms23031386 - 26 Jan 2022
Cited by 6 | Viewed by 3159
Abstract
The two crucial cellular insults that take place during cerebral ischemia are the loss of oxygen and loss of glucose, which can both activate a cascade of events leading to neuronal death. In addition, the toxic overactivation of neuronal excitatory receptors, leading to [...] Read more.
The two crucial cellular insults that take place during cerebral ischemia are the loss of oxygen and loss of glucose, which can both activate a cascade of events leading to neuronal death. In addition, the toxic overactivation of neuronal excitatory receptors, leading to Ca2+ overload, may contribute to ischemic neuronal injury. Brain ischemia can be simulated in vitro by oxygen/glucose deprivation, which can be reversible by the re-establishment of physiological conditions. Accordingly, we examined the effects of glucose deprivation on the PI3K/Akt survival signaling pathway and its crosstalk with HIF-1α and Ca2+ homeostasis in SH-SY5Y human neuroblastoma cells. It was found that glucose withdrawal decreased HIF-1α protein levels even in the presence of the ischemia-mimicking CoCl2. On the contrary, and despite neuronal death, we identified a strong activation of the master pro-survival kinase Akt, a finding that was also confirmed by the increased phosphorylation of GSK3, a direct target of p-Akt. Remarkably, the elevated Ca2+ influx recorded was found to promptly trigger the activation of Akt, while a re-addition of glucose resulted in rapid restoration of both Ca2+ entry and p-Akt levels, highlighting the plasticity of neurons to respond to ischemic challenges and the important role of glucose homeostasis for multiple neurological disorders. Full article
(This article belongs to the Special Issue Molecular Signaling in Stroke)
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27 pages, 4692 KiB  
Article
Transient Focal Cerebral Ischemia Leads to miRNA Alterations in Different Brain Regions, Blood Serum, Liver, and Spleen
by Clara Voelz, Nahal Ebrahimy, Weiyi Zhao, Pardes Habib, Adib Zendedel, Thomas Pufe, Cordian Beyer and Alexander Slowik
Int. J. Mol. Sci. 2022, 23(1), 161; https://doi.org/10.3390/ijms23010161 - 23 Dec 2021
Cited by 11 | Viewed by 3103
Abstract
Ischemic stroke is characterized by an occlusion of a cerebral blood vessel resulting in neuronal cell death due to nutritional and oxygen deficiency. Additionally, post-ischemic cell death is augmented after reperfusion. These events are paralleled by dysregulated miRNA expression profiles in the peri-infarct [...] Read more.
Ischemic stroke is characterized by an occlusion of a cerebral blood vessel resulting in neuronal cell death due to nutritional and oxygen deficiency. Additionally, post-ischemic cell death is augmented after reperfusion. These events are paralleled by dysregulated miRNA expression profiles in the peri-infarct area. Understanding the underlying molecular mechanism in the peri-infarct region is crucial for developing promising therapeutics. Utilizing a tMCAo (transient Middle Cerebral Artery occlusion) model in rats, we studied the expression levels of the miRNAs (miR) 223-3p, 155-5p, 3473, and 448-5p in the cortex, amygdala, thalamus, and hippocampus of both the ipsi- and contralateral hemispheres. Additionally, the levels in the blood serum, spleen, and liver and the expression of their target genes, namely, Nlrp3, Socs1, Socs3, and Vegfa, were assessed. We observed an increase in all miRNAs on the ipsilateral side of the cerebral cortex in a time-dependent manner and increased miRNAs levels (miR-223-3p, miR-3473, and miR-448-5p) in the contralateral hemisphere after 72 h. Besides the cerebral cortex, the amygdala presented increased expression levels, whereas the thalamus and hippocampus showed no alterations. Different levels of the investigated miRNAs were detected in blood serum, liver, and spleen. The gene targets were altered not only in the peri-infarct area of the cortex but selectively increased in the investigated non-affected brain regions along with the spleen and liver during the reperfusion time up to 72 h. Our results suggest a supra-regional influence of miRNAs following ischemic stroke, which should be studied to further identify whether miRNAs are transported or locally upregulated. Full article
(This article belongs to the Special Issue Molecular Signaling in Stroke)
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Review

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23 pages, 733 KiB  
Review
The Importance of Platelets Response during Antiplatelet Treatment after Ischemic Stroke—Between Benefit and Risk: A Systematic Review
by Joanna Sikora, Aleksandra Karczmarska-Wódzka, Joanna Bugieda and Przemysław Sobczak
Int. J. Mol. Sci. 2022, 23(3), 1043; https://doi.org/10.3390/ijms23031043 - 18 Jan 2022
Cited by 8 | Viewed by 2809
Abstract
Ischemic stroke is a disease related to abnormal blood flow that leads to brain dysfunction. The early and late phases of the disease are distinguished. A distinction is made between the early and late stages of the disease, and the best effect in [...] Read more.
Ischemic stroke is a disease related to abnormal blood flow that leads to brain dysfunction. The early and late phases of the disease are distinguished. A distinction is made between the early and late stages of the disease, and the best effect in treating an ischemic stroke is usually achieved within the first hours after the onset of symptoms. This review looked at studies platelet activity monitoring studies to determine the risks and benefits of various approaches including antiplatelet therapy. A study was conducted on recently published literature based on PRISMA. This review includes 32 research articles directly addressing the importance of monitoring platelet function during antiplatelet therapy (dual or monotherapy) after ischemic stroke. In patients with transient ischemic attack or ischemic stroke, antiplatelet therapy can reduce the risk of stroke by 11–15%, assuming that patients respond well. Secondary prevention results are dependent on platelet reactivity, meaning that patients do not respond equally to antiplatelet therapy. It is very important that aspirin-resistant patients can benefit from the use of dual antiplatelet therapy. The individualized approach to secondary stroke prevention is to administer the most appropriate drug at the correct dose and apply the optimal therapeutic procedure to the individual patient. Full article
(This article belongs to the Special Issue Molecular Signaling in Stroke)
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17 pages, 7137 KiB  
Review
Potential Role of Soluble Toll-like Receptors 2 and 4 as Therapeutic Agents in Stroke and Brain Hemorrhage
by Josh Lua, Kanishka Ekanayake, Madison Fangman and Sylvain Doré
Int. J. Mol. Sci. 2021, 22(18), 9977; https://doi.org/10.3390/ijms22189977 - 15 Sep 2021
Cited by 8 | Viewed by 3638
Abstract
Hemolysis is a physiological condition in which red blood cells (RBCs) lyse, releasing their contents into the extracellular environment. Hemolysis can be a manifestation of several diseases and conditions, such as sickle cell disease, hemorrhagic stroke, and trauma. Heme and hemoglobin are among [...] Read more.
Hemolysis is a physiological condition in which red blood cells (RBCs) lyse, releasing their contents into the extracellular environment. Hemolysis can be a manifestation of several diseases and conditions, such as sickle cell disease, hemorrhagic stroke, and trauma. Heme and hemoglobin are among the unique contents of RBCs that are released into the environment. Although these contents can cause oxidative stress, especially when oxidized in the extracellular environment, they can also initiate a proinflammatory response because they bind to receptors such as the Toll-like receptor (TLR) family. This review seeks to clarify the mechanism by which TLRs initiate a proinflammatory response to heme, hemoglobin, and their oxidized derivatives, as well as the possibility of using soluble TLRs (sTLRs) as therapeutic agents. Furthermore, this review explores the possibility of using sTLRs in hemorrhagic disorders in which mitigating inflammation is essential for clinical outcomes, including hemorrhagic stroke and its subtypes, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). Full article
(This article belongs to the Special Issue Molecular Signaling in Stroke)
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