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Cells
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The Role of Neural Stem/Progenitor Cells in Neurological Diseases
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The Role of Neural Stem/Progenitor Cells in Neurological Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 4925

Special Issue Editor

Dr. Jisook Moon

E-Mail Website
Guest Editor
Department of Biotechnology, CHA University, CHABioComplex, 335, Pangyo-ro, Bundang-gu, Seongnam-si, Gyeonggi-do, Republic of Korea
Interests: neuroscience; Alzhimer's diseases; Parkinson's diseases; senescence; cell biology; stem cells; extracellular vesicles; biomarker bioinformatics; statistics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neural stem progenitor cells (NSPCs), self-renewing multipotent cells, persist from embryogenesis and are capable of differentiation into neurons, astrocytes, and oligodendrocytes. Because their proliferation and differentiation are tightly controlled in brain development, the disturbance of NSPC biology is responsible for various neurological diseases, from developmental and psychiatric disorders to degenerative diseases and cancers in adults. In addition, NSPCs carefully develop cell therapies for diverse neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s diseases, and the transplantations of NSPCs through different routes are performed in order to recover the pathophysiological deficits in the diseases. Since NSPCs can be generated from induced pluripotent stem cells, the cell applications are expanded to neural tissue engineering with a three-dimensional culture system and development of personalized neurotoxic tests and therapies, which help us find new interventions and understand the underlying mechanisms of neurological diseases. Both NSPCs themselves and the derivatives from the cells, including conditioned media, secreted factors, and extracellular vesicles, are under intensive investigation to understand the NSPC-mediated modulation of neuronal diseases. Because of their different roles in neurological disorders, diverse approaches of NSPC investigation are required for comprehending the nature of NSPCs.

This Special Issue aims to expand the current knowledge on the roles of NSPCs and their derivatives in neurological diseases from the pathological mechanism to the possible therapeutic mechanism, and from new applications to development of noble interventions. 
We look forward to your contributions. 

Dr. Jisook Moon
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neural stem/progenitor cells (NSPCs)
  • neurological diseases
  • neurodegenerative diseases
  • cancers
  • pathophysiological mechanism
  • NSPC derivatives
  • conditioned media
  • secreted factors
  • extracellular vesicles
  • therapeutic intervention

Published Papers (3 papers)

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Research

21 pages, 4657 KiB  
Article
Tpr Misregulation in Hippocampal Neural Stem Cells in Mouse Models of Alzheimer’s Disease
by Subash C. Malik, Jia-Di Lin, Stephanie Ziegler-Waldkirch, Stefan Tholen, Sachin S. Deshpande, Marius Schwabenland, Oliver Schilling, Andreas Vlachos, Melanie Meyer-Luehmann and Christian Schachtrup
Cells 2023, 12(23), 2757; https://doi.org/10.3390/cells12232757 - 01 Dec 2023
Viewed by 1276
Abstract
Nuclear pore complexes (NPCs) are highly dynamic macromolecular protein structures that facilitate molecular exchange across the nuclear envelope. Aberrant NPC functioning has been implicated in neurodegeneration. The translocated promoter region (Tpr) is a critical scaffolding nucleoporin (Nup) of the nuclear basket, facing the [...] Read more.
Nuclear pore complexes (NPCs) are highly dynamic macromolecular protein structures that facilitate molecular exchange across the nuclear envelope. Aberrant NPC functioning has been implicated in neurodegeneration. The translocated promoter region (Tpr) is a critical scaffolding nucleoporin (Nup) of the nuclear basket, facing the interior of the NPC. However, the role of Tpr in adult neural stem/precursor cells (NSPCs) in Alzheimer’s disease (AD) is unknown. Using super-resolution (SR) and electron microscopy, we defined the different subcellular localizations of Tpr and phospho-Tpr (P-Tpr) in NSPCs in vitro and in vivo. Elevated Tpr expression and reduced P-Tpr nuclear localization accompany NSPC differentiation along the neurogenic lineage. In 5xFAD mice, an animal model of AD, increased Tpr expression in DCX+ hippocampal neuroblasts precedes increased neurogenesis at an early stage, before the onset of amyloid-β plaque formation. Whereas nuclear basket Tpr interacts with chromatin modifiers and NSPC-related transcription factors, P-Tpr interacts and co-localizes with cyclin-dependent kinase 1 (Cdk1) at the nuclear chromatin of NSPCs. In hippocampal NSPCs in a mouse model of AD, aberrant Tpr expression was correlated with altered NPC morphology and counts, and Tpr was aberrantly expressed in postmortem human brain samples from patients with AD. Thus, we propose that altered levels and subcellular localization of Tpr in CNS disease affect Tpr functionality, which in turn regulates the architecture and number of NSPC NPCs, possibly leading to aberrant neurogenesis. Full article
(This article belongs to the Special Issue The Role of Neural Stem/Progenitor Cells in Neurological Diseases)
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20 pages, 5719 KiB  
Article
Microglia Negatively Regulate the Proliferation and Neuronal Differentiation of Neural Stem/Progenitor Cells Isolated from Poststroke Mouse Brains
by Yoshinobu Hirano, Takayuki Nakagomi, Akiko Nakano-Doi, Shuji Kubo, Yusuke Minato, Toshinori Sawano, Masafumi Sakagami and Kenzo Tsuzuki
Cells 2023, 12(16), 2040; https://doi.org/10.3390/cells12162040 - 10 Aug 2023
Cited by 1 | Viewed by 1216
Abstract
We previously demonstrated that neural stem/progenitor cells (NSPCs) were induced within and around the ischemic areas in a mouse model of ischemic stroke. These injury/ischemia-induced NSPCs (iNSPCs) differentiated to electrophysiologically functional neurons in vitro, indicating the presence of a self-repair system following injury. [...] Read more.
We previously demonstrated that neural stem/progenitor cells (NSPCs) were induced within and around the ischemic areas in a mouse model of ischemic stroke. These injury/ischemia-induced NSPCs (iNSPCs) differentiated to electrophysiologically functional neurons in vitro, indicating the presence of a self-repair system following injury. However, during the healing process after stroke, ischemic areas were gradually occupied by inflammatory cells, mainly microglial cells/macrophages (MGs/MΦs), and neurogenesis rarely occurred within and around the ischemic areas. Therefore, to achieve neural regeneration by utilizing endogenous iNSPCs, regulation of MGs/MΦs after an ischemic stroke might be necessary. To test this hypothesis, we used iNSPCs isolated from the ischemic areas after a stroke in our mouse model to investigate the role of MGs/MΦs in iNSPC regulation. In coculture experiments, we show that the presence of MGs/MΦs significantly reduces not only the proliferation but also the differentiation of iNSPCs toward neuronal cells, thereby preventing neurogenesis. These effects, however, are mitigated by MG/MΦ depletion using clodronate encapsulated in liposomes. Additionally, gene ontology analysis reveals that proliferation and neuronal differentiation are negatively regulated in iNSPCs cocultured with MGs/MΦs. These results indicate that MGs/MΦs negatively impact neurogenesis via iNSPCs, suggesting that the regulation of MGs/MΦs is essential to achieve iNSPC-based neural regeneration following an ischemic stroke. Full article
(This article belongs to the Special Issue The Role of Neural Stem/Progenitor Cells in Neurological Diseases)
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20 pages, 27279 KiB  
Article
The Role and Mechanism of Transglutaminase 2 in Regulating Hippocampal Neurogenesis after Traumatic Brain Injury
by Ruo-Xi Shi, Cong Liu, Ya-Jie Xu, Ying-Ying Wang, Bao-Dong He, Xuan-Cheng He, Hong-Zhen Du, Baoyang Hu, Jianwei Jiao, Chang-Mei Liu and Zhao-Qian Teng
Cells 2023, 12(4), 558; https://doi.org/10.3390/cells12040558 - 09 Feb 2023
Cited by 5 | Viewed by 1935
Abstract
Traumatic brain injury usually results in neuronal loss and cognitive deficits. Promoting endogenous neurogenesis has been considered as a viable treatment option to improve functional recovery after TBI. However, neural stem/progenitor cells (NSPCs) in neurogenic regions are often unable to migrate and differentiate [...] Read more.
Traumatic brain injury usually results in neuronal loss and cognitive deficits. Promoting endogenous neurogenesis has been considered as a viable treatment option to improve functional recovery after TBI. However, neural stem/progenitor cells (NSPCs) in neurogenic regions are often unable to migrate and differentiate into mature neurons at the injury site. Transglutaminase 2 (TGM2) has been identified as a crucial component of neurogenic niche, and significantly dysregulated after TBI. Therefore, we speculate that TGM2 may play an important role in neurogenesis after TBI, and strategies targeting TGM2 to promote endogenous neural regeneration may be applied in TBI therapy. Using a tamoxifen-induced Tgm2 conditional knockout mouse line and a mouse model of stab wound injury, we investigated the role and mechanism of TGM2 in regulating hippocampal neurogenesis after TBI. We found that Tgm2 was highly expressed in adult NSPCs and up-regulated after TBI. Conditional deletion of Tgm2 resulted in the impaired proliferation and differentiation of NSPCs, while Tgm2 overexpression enhanced the abilities of self-renewal, proliferation, differentiation, and migration of NSPCs after TBI. Importantly, injection of lentivirus overexpressing TGM2 significantly promoted hippocampal neurogenesis after TBI. Therefore, TGM2 is a key regulator of hippocampal neurogenesis and a pivotal therapeutic target for intervention following TBI. Full article
(This article belongs to the Special Issue The Role of Neural Stem/Progenitor Cells in Neurological Diseases)
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