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Molecular Mechanisms of Brain Repair and Restoration after Stroke
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Molecular Mechanisms of Brain Repair and Restoration after Stroke

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

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 28170

Special Issue Editor

Dr. Valentina Arnao

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Guest Editor
Department of Biomedicine, Neuroscience and Advanced Diagnostics (BiND), University of Palermo, Via Gaetano la Loggia n.1, 90129 Palermo, Italy
Interests: stroke; extrapiramidal syndromes; sex differences in neurological disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the results achieved by available reperfusion therapies, the outcomes after a stroke often remain poor. It has been observed that the restoration of pre-injury connections or the recruitment of new ones can encourage spontaneous functional recovery in days, weeks, or months. Neuroplasticity, as an intrinsic property of the brain in response to external and internal injuries and that allows functional and structural reorganization, is key to regeneration after injury. However, spontaneous recovery after a stroke is generally incomplete and depends on the ability of the brain to reestablish the structural and functional organization of neurovascular networks. It has been observed that not only are neurons actively involved in this process, but so are astrocytes, microglia, and cerebrovascular cells/cerebral vessels. Post-stroke neuroangiogenesis properties, such as inflammation, have been recognized as a compensatory mechanism to repair the damage caused by a stroke.

This Special Issue of the International Journal of Molecular Sciences aims to provide news regarding the mechanisms of brain restoration after a stroke. A better knowledge of brain repair mechanisms is essential to enhance said mechanisms and to improve the functional outcome of a patient after a stroke. Moreover, neuroplasticity could be maladaptive when resulting in negative effects such as loss of function. The information on the neurobiology of brain restoration may help to develop new therapies that enhance brain recovery after a stroke and that reduce maladaptive effects. Submissions highlighting each of these topics are welcome.

Dr. Valentina Arnao
Guest Editor

Manuscript Submission Information

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Keywords

  • Stroke
  • Brain repair
  • Restoration
  • Neuroplasticity
  • Rehabilitation after stroke
  • Inflammation
  • Neuroangiogenesis

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Published Papers (5 papers)

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Research

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16 pages, 3082 KiB  
Article
Brain Protein Expression Profile Confirms the Protective Effect of the ACTH(4–7)PGP Peptide (Semax) in a Rat Model of Cerebral Ischemia–Reperfusion
by Olga Yu. Sudarkina, Ivan B. Filippenkov, Vasily V. Stavchansky, Alina E. Denisova, Vadim V. Yuzhakov, Larisa E. Sevan’kaeva, Liya V. Valieva, Julia A. Remizova, Veronika G. Dmitrieva, Leonid V. Gubsky, Nikolai F. Myasoedov, Svetlana A. Limborska and Lyudmila V. Dergunova
Int. J. Mol. Sci. 2021, 22(12), 6179; https://doi.org/10.3390/ijms22126179 - 8 Jun 2021
Cited by 9 | Viewed by 4215
Abstract
The Semax (Met-Glu-His-Phe-Pro-Gly-Pro) peptide is a synthetic melanocortin derivative that is used in the treatment of ischemic stroke. Previously, studies of the molecular mechanisms underlying the actions of Semax using models of cerebral ischemia in rats showed that the peptide enhanced the transcription [...] Read more.
The Semax (Met-Glu-His-Phe-Pro-Gly-Pro) peptide is a synthetic melanocortin derivative that is used in the treatment of ischemic stroke. Previously, studies of the molecular mechanisms underlying the actions of Semax using models of cerebral ischemia in rats showed that the peptide enhanced the transcription of neurotrophins and their receptors and modulated the expression of genes involved in the immune response. A genome-wide RNA-Seq analysis revealed that, in the rat transient middle cerebral artery occlusion (tMCAO) model, Semax suppressed the expression of inflammatory genes and activated the expression of neurotransmitter genes. Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke. At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax. Moreover, a regulatory network was constructed. In conclusion, the suppression of inflammatory and cell death processes and the activation of recovery may contribute to the neuroprotective action of Semax at both the transcriptome and protein levels. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Brain Repair and Restoration after Stroke)
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Review

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23 pages, 3966 KiB  
Review
Neuroinflammation and COVID-19 Ischemic Stroke Recovery—Evolving Evidence for the Mediating Roles of the ACE2/Angiotensin-(1–7)/Mas Receptor Axis and NLRP3 Inflammasome
by Che Mohd Nasril Che Mohd Nassir, Mohd K. I. Zolkefley, Muhammad Danial Ramli, Haziq Hazman Norman, Hafizah Abdul Hamid and Muzaimi Mustapha
Int. J. Mol. Sci. 2022, 23(6), 3085; https://doi.org/10.3390/ijms23063085 - 13 Mar 2022
Cited by 16 | Viewed by 4684
Abstract
Cerebrovascular events, notably acute ischemic strokes (AIS), have been reported in the setting of novel coronavirus disease (COVID-19) infection. Commonly regarded as cryptogenic, to date, the etiology is thought to be multifactorial and remains obscure; it is linked either to a direct viral [...] Read more.
Cerebrovascular events, notably acute ischemic strokes (AIS), have been reported in the setting of novel coronavirus disease (COVID-19) infection. Commonly regarded as cryptogenic, to date, the etiology is thought to be multifactorial and remains obscure; it is linked either to a direct viral invasion or to an indirect virus-induced prothrombotic state, with or without the presence of conventional cerebrovascular risk factors. In addition, patients are at a greater risk of developing long-term negative sequelae, i.e., long-COVID-related neurological problems, when compared to non-COVID-19 stroke patients. Central to the underlying neurobiology of stroke recovery in the context of COVID-19 infection is reduced angiotensin-converting enzyme 2 (ACE2) expression, which is known to lead to thrombo-inflammation and ACE2/angiotensin-(1–7)/mitochondrial assembly receptor (MasR) (ACE2/Ang-(1-7)/MasR) axis inhibition. Moreover, after AIS, the activated nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome may heighten the production of numerous proinflammatory cytokines, mediating neuro-glial cell dysfunction, ultimately leading to nerve-cell death. Therefore, potential neuroprotective therapies targeting the molecular mechanisms of the aforementioned mediators may help to inform rehabilitation strategies to improve brain reorganization (i.e., neuro-gliogenesis and synaptogenesis) and secondary prevention among AIS patients with or without COVID-19. Therefore, this narrative review aims to evaluate the mediating role of the ACE2/Ang- (1-7)/MasR axis and NLRP3 inflammasome in COVID-19-mediated AIS, as well as the prospects of these neuroinflammation mediators for brain repair and in secondary prevention strategies against AIS in stroke rehabilitation. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Brain Repair and Restoration after Stroke)
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16 pages, 1245 KiB  
Review
Rho/ROCK Pathway and Noncoding RNAs: Implications in Ischemic Stroke and Spinal Cord Injury
by Tetsu Kimura, Yuta Horikoshi, Chika Kuriyagawa and Yukitoshi Niiyama
Int. J. Mol. Sci. 2021, 22(21), 11573; https://doi.org/10.3390/ijms222111573 - 26 Oct 2021
Cited by 30 | Viewed by 5430
Abstract
Ischemic strokes (IS) and spinal cord injuries (SCI) are major causes of disability. RhoA is a small GTPase protein that activates a downstream effector, ROCK. The up-regulation of the RhoA/ROCK pathway contributes to neuronal apoptosis, neuroinflammation, blood-brain barrier dysfunction, astrogliosis, and axon growth [...] Read more.
Ischemic strokes (IS) and spinal cord injuries (SCI) are major causes of disability. RhoA is a small GTPase protein that activates a downstream effector, ROCK. The up-regulation of the RhoA/ROCK pathway contributes to neuronal apoptosis, neuroinflammation, blood-brain barrier dysfunction, astrogliosis, and axon growth inhibition in IS and SCI. Noncoding RNAs (ncRNAs), such as microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), were previously considered to be non-functional. However, they have attracted much attention because they play an essential role in regulating gene expression in physiological and pathological conditions. There is growing evidence that ROCK inhibitors, such as fasudil and VX-210, can reduce injury in IS and SCI in animal models and clinical trials. Recently, it has been reported that miRNAs are decreased in IS and SCI, while lncRNAs are increased. Inhibiting the Rho/ROCK pathway with miRNAs alleviates apoptosis, neuroinflammation, oxidative stress, and axon growth inhibition in IS and SCI. Further studies are required to explore the significance of ncRNAs in IS and SCI and to establish new strategies for preventing and treating these devastating diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Brain Repair and Restoration after Stroke)
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21 pages, 1746 KiB  
Review
Repair Mechanisms of the Neurovascular Unit after Ischemic Stroke with a Focus on VEGF
by Sunhong Moon, Mi-Sook Chang, Seong-Ho Koh and Yoon Kyung Choi
Int. J. Mol. Sci. 2021, 22(16), 8543; https://doi.org/10.3390/ijms22168543 - 9 Aug 2021
Cited by 53 | Viewed by 7588
Abstract
The functional neural circuits are partially repaired after an ischemic stroke in the central nervous system (CNS). In the CNS, neurovascular units, including neurons, endothelial cells, astrocytes, pericytes, microglia, and oligodendrocytes maintain homeostasis; however, these cellular networks are damaged after an ischemic stroke. [...] Read more.
The functional neural circuits are partially repaired after an ischemic stroke in the central nervous system (CNS). In the CNS, neurovascular units, including neurons, endothelial cells, astrocytes, pericytes, microglia, and oligodendrocytes maintain homeostasis; however, these cellular networks are damaged after an ischemic stroke. The present review discusses the repair potential of stem cells (i.e., mesenchymal stem cells, endothelial precursor cells, and neural stem cells) and gaseous molecules (i.e., nitric oxide and carbon monoxide) with respect to neuroprotection in the acute phase and regeneration in the late phase after an ischemic stroke. Commonly shared molecular mechanisms in the neurovascular unit are associated with the vascular endothelial growth factor (VEGF) and its related factors. Stem cells and gaseous molecules may exert therapeutic effects by diminishing VEGF-mediated vascular leakage and facilitating VEGF-mediated regenerative capacity. This review presents an in-depth discussion of the regeneration ability by which endogenous neural stem cells and endothelial cells produce neurons and vessels capable of replacing injured neurons and vessels in the CNS. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Brain Repair and Restoration after Stroke)
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14 pages, 500 KiB  
Review
Biomarkers of Angiogenesis and Neuroplasticity as Promising Clinical Tools for Stroke Recovery Evaluation
by Lidia Wlodarczyk, Rafal Szelenberger, Natalia Cichon, Joanna Saluk-Bijak, Michal Bijak and Elzbieta Miller
Int. J. Mol. Sci. 2021, 22(8), 3949; https://doi.org/10.3390/ijms22083949 - 11 Apr 2021
Cited by 24 | Viewed by 4667
Abstract
Several key issues impact the clinical practice of stroke rehabilitation including a patient’s medical history, stroke experience, the potential for recovery, and the selection of the most effective type of therapy. Until clinicians have answers to these concerns, the treatment and rehabilitation are [...] Read more.
Several key issues impact the clinical practice of stroke rehabilitation including a patient’s medical history, stroke experience, the potential for recovery, and the selection of the most effective type of therapy. Until clinicians have answers to these concerns, the treatment and rehabilitation are rather intuitive, with standard procedures carried out based on subjective estimations using clinical scales. Therefore, there is a need to find biomarkers that could predict brain recovery potential in stroke patients. This review aims to present the current state-of-the-art stroke recovery biomarkers that could be used in clinical practice. The revision of biochemical biomarkers has been developed based on stroke recovery processes: angiogenesis and neuroplasticity. This paper provides an overview of the biomarkers that are considered to be ready-to-use in clinical practice and others, considered as future tools. Furthermore, this review shows the utility of biomarkers in the development of the concept of personalized medicine. Enhancing brain neuroplasticity and rehabilitation facilitation are crucial concerns not only after stroke, but in all central nervous system diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Brain Repair and Restoration after Stroke)
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