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Molecular Research on Neuronal Cell Death and Neurogenesis
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Molecular Research on Neuronal Cell Death and Neurogenesis

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 (20 March 2025) | Viewed by 8446

Special Issue Editor

Dr. Theologos Michaelidis

E-Mail Website
Guest Editor
1. Department of Biological Applications and Technologies, School of Health Sciences, University of Ioannina, 45110 Ioannina, Greece
2. Biomedical Research Institute, Foundation for Research and Technology-Hellas, 45500 Ioannina, Greece
Interests: molecular biology; programmed cell death; neurogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurogenesis is the process by which cells of the nervous system, called neurons, are generated from neural stem cells (NSCs). In 1842, Karl Vogt first noted the requirement for physiological cell death when studying metamorphosis of amphibians. Neuronal cell death was first noticed as a loss of neurons during development. Neuronal death is normal during nervous system development but is abnormal in brain and spinal cord disease and injury. Neuronal cell death occurs extensively during development and pathology. We now know that neurons die in at least a dozen ways, including apoptosis and necrosis, etc. A better understanding of the molecular mechanisms of neuronal cell death in nervous system development, injury and disease can lead to new therapeutic approaches for the prevention of neurodegeneration and neurological disabilities and will expand the field of cell death biology.

The purpose of this special issue is to present the latest research on the molecular mechanisms of neuronal cell death and neurogenesis, and the available evidence suggesting a possible role of different forms of cell death in the pathogenesis of neurological diseases. Both original research articles and comprehensive reviews are welcomed.

Dr. Theologos Michaelidis
Guest Editor

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Published Papers (3 papers)

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Research

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20 pages, 4922 KiB  
Article
The 419th Aspartic Acid of Neural Membrane Protein Enolase 2 Is a Key Residue Involved in the Axonal Growth of Motor Neurons Mediated by Interaction between Enolase 2 Receptor and Extracellular Pgk1 Ligand
by Bing-Chang Lee, Jui-Che Tsai, Yi-Hsin Huang, Chun-Cheng Wang, Hung-Chieh Lee and Huai-Jen Tsai
Int. J. Mol. Sci. 2024, 25(19), 10753; https://doi.org/10.3390/ijms251910753 - 6 Oct 2024
Cited by 1 | Viewed by 1541
Abstract
Neuron-specific Enolase 2 (Eno2) is an isozyme primarily distributed in the central and peripheral nervous systems and neuroendocrine cells. It promotes neuronal survival, differentiation, and axonal regeneration. Recent studies have shown that Eno2 localized on the cell membrane of motor neurons acts as [...] Read more.
Neuron-specific Enolase 2 (Eno2) is an isozyme primarily distributed in the central and peripheral nervous systems and neuroendocrine cells. It promotes neuronal survival, differentiation, and axonal regeneration. Recent studies have shown that Eno2 localized on the cell membrane of motor neurons acts as a receptor for extracellular phosphoglycerate kinase 1 (ePgk1), which is secreted by muscle cells and promotes the neurite outgrowth of motor neurons (NOMN). However, interaction between Eno1, another isozyme of Enolase, and ePgk1 failed to return the same result. To account for the difference, we constructed seven point-mutations of Eno2, corresponding to those of Eno1, and verified their effects on NOMN. Among the seven Eno2 mutants, eno2-siRNA-knockdown NSC34 cells transfected with plasmid encoding the 419th aspartic acid mutated into serine (Eno2-[D419S]) or Eno2-[E420K] showed a significant reduction in neurite length. Moreover, the Eno2-ePgk1-interacted synergic effect on NOMN driven by Eno2-[D419S] was more profoundly reduced than that driven by Eno2-[E420K], suggesting that D419 was the more essential residue involved in NOMN mediated by Eno2-ePgk1 interaction. Eno2-ePgk1-mediated NOMN appeared to increase the level of p-Cofilin, a growth cone collapse marker, in NSC34 cells transfected with Eno2-[D419S] and incubated with ePgk1, thereby inhibiting NOMN. Furthermore, we conducted in vivo experiments using zebrafish transgenic line Tg(mnx1:GFP), in which GFP is tagged in motor neurons. In the presence of ePgk1, the retarded growth of axons in embryos injected with eno2-specific antisense morpholino oligonucleotides (MO) could be rescued by wobble-eno2-mRNA. However, despite the addition of ePgk1, the decreased defective axons and the increased branched neurons were not significantly improved in the eno2-[D419S]-mRNA-injected embryos. Collectively, these results lead us to suggest that the 419th aspartic acid of mouse Eno2 is likely a crucial site affecting motor neuron development mediated by Eno2-ePgk1 interaction, and, hence, mutations result in a significant reduction in the degree of NOMN in vitro and axonal growth in vivo. Full article
(This article belongs to the Special Issue Molecular Research on Neuronal Cell Death and Neurogenesis)
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21 pages, 8481 KiB  
Article
Cellular Therapy in Experimental Autoimmune Encephalomyelitis as an Adjuvant Treatment to Translate for Multiple Sclerosis
by Maiara Carolina Perussolo, Bassam Felipe Mogharbel, Cláudia Sayuri Saçaki, Nádia Nascimento da Rosa, Ana Carolina Irioda, Nathalia Barth de Oliveira, Julia Maurer Appel, Larissa Lührs, Leanderson Franco Meira, Luiz Cesar Guarita-Souza, Seigo Nagashima, Caroline Busatta Vaz de Paula, Lucia de Noronha, Idiberto José Zotarelli-Filho, Eltyeb Abdelwahid and Katherine Athayde Teixeira de Carvalho
Int. J. Mol. Sci. 2024, 25(13), 6996; https://doi.org/10.3390/ijms25136996 - 26 Jun 2024
Cited by 1 | Viewed by 1845
Abstract
This study aims to evaluate and compare cellular therapy with human Wharton’s jelly (WJ) mesenchymal stem cells (MSCs) and neural precursors (NPs) in experimental autoimmune encephalomyelitis (EAE), a preclinical model of Multiple Sclerosis. MSCs were isolated from WJ by an explant technique, differentiated [...] Read more.
This study aims to evaluate and compare cellular therapy with human Wharton’s jelly (WJ) mesenchymal stem cells (MSCs) and neural precursors (NPs) in experimental autoimmune encephalomyelitis (EAE), a preclinical model of Multiple Sclerosis. MSCs were isolated from WJ by an explant technique, differentiated to NPs, and characterized by cytometry and immunocytochemistry analysis after ethical approval. Forty-eight rats were EAE-induced by myelin basic protein and Freund’s complete adjuvant. Forty-eight hours later, the animals received intraperitoneal injections of 250 ng/dose of Bordetella pertussis toxin. Fourteen days later, the animals were divided into the following groups: a. non-induced, induced: b. Sham, c. WJ-MSCs, d. NPs, and e. WJ-MSCs plus NPs. 1 × 105. Moreover, the cells were placed in a 10 µL solution and injected via a stereotaxic intracerebral ventricular injection. After ten days, the histopathological analysis for H&E, Luxol, interleukins, and CD4/CD8 was carried out. Statistical analyses demonstrated a higher frequency of clinical manifestation in the Sham group (15.66%) than in the other groups; less demyelination was seen in the treated groups than the Sham group (WJ-MSCs, p = 0.016; NPs, p = 0.010; WJ-MSCs + NPs, p = 0.000), and a lower cellular death rate was seen in the treated groups compared with the Sham group. A CD4/CD8 ratio of <1 showed no association with microglial activation (p = 0.366), astrocytes (p = 0.247), and cell death (p = 0.577) in WJ-MSCs. WJ-MSCs and NPs were immunomodulatory and neuroprotective in cellular therapy, which would be translated as an adjunct in demyelinating diseases. Full article
(This article belongs to the Special Issue Molecular Research on Neuronal Cell Death and Neurogenesis)
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Review

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24 pages, 384 KiB  
Review
Neuroprotection during Thrombectomy for Acute Ischemic Stroke: A Review of Future Therapies
by Vikalpa Dammavalam, Sandra Lin, Sayedatun Nessa, Neil Daksla, Kamil Stefanowski, Ana Costa and Sergio Bergese
Int. J. Mol. Sci. 2024, 25(2), 891; https://doi.org/10.3390/ijms25020891 - 10 Jan 2024
Cited by 14 | Viewed by 4175
Abstract
Stroke is a major cause of death and disability worldwide. Endovascular thrombectomy has been impactful in decreasing mortality. However, many clinical results continue to show suboptimal functional outcomes despite high recanalization rates. This gap in recanalization and symptomatic improvement suggests a need for [...] Read more.
Stroke is a major cause of death and disability worldwide. Endovascular thrombectomy has been impactful in decreasing mortality. However, many clinical results continue to show suboptimal functional outcomes despite high recanalization rates. This gap in recanalization and symptomatic improvement suggests a need for adjunctive therapies in post-thrombectomy care. With greater insight into ischemia-reperfusion injury, recent preclinical testing of neuroprotective agents has shifted towards preventing oxidative stress through upregulation of antioxidants and downstream effectors, with positive results. Advances in multiple neuroprotective therapies, including uric acid, activated protein C, nerinetide, otaplimastat, imatinib, verapamil, butylphthalide, edaravone, nelonemdaz, ApTOLL, regional hypothermia, remote ischemic conditioning, normobaric oxygen, and especially nuclear factor erythroid 2-related factor 2, have promising evidence for improving stroke care. Sedation and blood pressure management in endovascular thrombectomy also play crucial roles in improved stroke outcomes. A hand-in-hand approach with both endovascular therapy and neuroprotection may be the key to targeting disability due to stroke. Full article
(This article belongs to the Special Issue Molecular Research on Neuronal Cell Death and Neurogenesis)
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