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New Molecular Progression of Stem Cell Therapy for Neurological Disorders
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New Molecular Progression of Stem Cell Therapy for Neurological Disorders

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: 25 June 2024 | Viewed by 2167

Special Issue Editor

Prof. Dr. Changmei Liu

E-Mail Website
Guest Editor
State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China
Interests: epigenetics; neurogenesis; neurodevelopment; regenerative medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Stem cell therapies have high potential as an emerging biopharmaceutical paradigm for most neurological disorders, such as Parkinsonism, schizophrenia, Alzheimer's disease, epilepsy, autism spectrum disorder, and brain injuries, either by using the cells or their secretome. However, there is still a lot to uncover regarding the therapeutic mechanisms based on stem cells. Greater understanding of these mechanisms will facilitate the optimization of cell-based therapies for neurological disorders.

This Special Issue aims to provide a more comprehensive overview of the role of stem cells in neurological disorders. Therefore, we welcome high-quality original research manuscripts, reviews, methods, and perspectives on topics related to new molecular progressions of stem cell therapy for neurological disorders, especially neural stem cells, including but not limited to (1) endogenous neurogenesis stimulation; (2) neural stem cell transplantation; (3) transdifferentiation; and (4) supportive mechanism for endogenous or transplanted neural stem cells. We also welcome therapeutic approaches based on stem cells using either cells or their secretome with the native or genetically engineered forms, in combination or not with biomaterials. Novel therapeutic trials using neural stem cells as well as engineering protocols that help cells to survive or to reach the brain will also be considered.

Prof. Dr. Changmei Liu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Published Papers (2 papers)

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Research

11 pages, 1547 KiB  
Article
Early-Stage Application of Agomir-137 Promotes Locomotor Recovery in a Mouse Model of Motor Cortex Injury
by Xiao-Tian Liu and Zhao-Qian Teng
Int. J. Mol. Sci. 2023, 24(24), 17156; https://doi.org/10.3390/ijms242417156 - 05 Dec 2023
Viewed by 627
Abstract
Traumatic brain injury (TBI) is a significant risk factor for neurodegenerative disorders, and patients often experience varying degrees of motor impairment. MiR-137, a broadly conserved and brain-enriched miRNA, is a key regulator in neural development and in various neurological diseases. Following TBI, the [...] Read more.
Traumatic brain injury (TBI) is a significant risk factor for neurodegenerative disorders, and patients often experience varying degrees of motor impairment. MiR-137, a broadly conserved and brain-enriched miRNA, is a key regulator in neural development and in various neurological diseases. Following TBI, the expression of miR-137 is dramatically downregulated. However, whether miR-137 is a therapeutic target for TBI still remains unknown. Here, for the first time, we demonstrate that intranasal administration of miR-137 agomir (a mimic) in the early stage (0–7 days) of TBI effectively inhibits glial scar formation and improves neuronal survival, while early-stage administration of miR-137 antagomir (an inhibitor) deteriorates motor impairment. This study elucidates the therapeutic potential of miR-137 mimics in improving locomotor recovery following motor cortex injury. Full article
(This article belongs to the Special Issue New Molecular Progression of Stem Cell Therapy for Neurological Disorders)
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14 pages, 1994 KiB  
Article
A Human Brain Model Mimicking Umbilical Cord Mesenchymal Stem Cells for the Treatment of Hypoxic-Ischemic Brain Injury
by Xidan Li, Haijing Liu, Chao Han, Jianglin Luo, Xin Guan, Liang Wang, Ying Li, Jiayi Wang, Hua Piao, Wei Zou and Jing Liu
Int. J. Mol. Sci. 2023, 24(18), 14208; https://doi.org/10.3390/ijms241814208 - 18 Sep 2023
Viewed by 992
Abstract
We used an in vitro model of the human brain immune microenvironment to simulate hypoxic-ischemic brain injury (HIBI) and treatment with human umbilical cord mesenchymal stem cells (hUMSCs) to address the transformation barriers of gene differences between animals and humans in preclinical research. [...] Read more.
We used an in vitro model of the human brain immune microenvironment to simulate hypoxic-ischemic brain injury (HIBI) and treatment with human umbilical cord mesenchymal stem cells (hUMSCs) to address the transformation barriers of gene differences between animals and humans in preclinical research. A co-culture system, termed hNAME, consisted of human hippocampal neurons (N), astrocytes (A), microglia (M), and brain microvascular endothelial cells (E). Flow cytometry measured the apoptosis rates of neurons and endothelial cells. hNAME-neurons and endothelial cells experienced more severe damage than monolayer cells, particularly after 48 h and 24 h of reoxygenation (OGD48/R24). Western blotting identified neuroinflammatory response markers, including HIF-1α, C1q, C3, TNF-α, and iNOS. Inflammatory factors originated from the glial chamber rather than the neurons and vascular endothelial chambers. A gradual increase in the release of inflammatory factors was observed as the OGD and reoxygenation times increased, peaking at OGD48/R24. The hNAME value was confirmed in human umbilical cord mesenchymal stem cells (hUMSCs). Treatment with hUMSCs resulted in a notable decrease in the severity of neuronal and endothelial cell damage in hNAME. The hNAME is an ideal in vitro model for simulating the immune microenvironment of the human brain because of the interactions between neurons, vessels, astrocytes, and microglia. Full article
(This article belongs to the Special Issue New Molecular Progression of Stem Cell Therapy for Neurological Disorders)
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