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Therapeutic Mechanisms of Stem Cells and Exosomes for Geriatric Disease
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Therapeutic Mechanisms of Stem Cells and Exosomes for Geriatric Disease

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 2023) | Viewed by 5974

Special Issue Editor

Dr. Dongsun Park

E-Mail Website
Guest Editor
Department of Biology Education, Korea National University of Education, Cheongju 28173, Republic of Korea
Interests: stem cells; exosomes; geriatric disease; neurodegenerative disease; strokes; aging

Special Issue Information

Dear Colleagues,

As we enter an aging society, we are observing an increasing number of geriatric diseases, such as neurodegenerative diseases and strokes. Many treatments are being developed to deal with these diseases; however, effective treatments do not yet exist. Natural drugs, therapeutic antibodies, and small molecules are also attracting attention as new treatments, but the most popular candidates are stem cells and exosomes. In fact, many preclinical studies have reported numerous therapeutic effects of stem cells and exosomes; however, clinical use is still insufficient.

One of the reasons for this is probably because the therapeutic mechanism of stem cells is not clear, and in the case of exosomes, the mechanisms of generation and composition are not clear. In addition, for the efficient treatment of diseases, their treatment mechanisms must be clearly identified.

The purpose of this issue is to emphasize the molecular mechanisms of stem cells and exosomes and the role of various molecules in the process, as well as the direction in which these treatments will proceed in the future. Original research articles, review articles, and short communications in the research areas described (but not limited to) are welcome.

Dr. Dongsun Park
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.

Keywords

  • stem cells
  • exosomes
  • geriatric disease
  • neurodegenerative disease
  • strokes
  • aging

Published Papers (2 papers)

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Research

23 pages, 8278 KiB  
Article
Extracellular Vesicle Treatment Alleviates Neurodevelopmental and Neurodegenerative Pathology in Cortical Spheroid Model of Down Syndrome
by Natalie Baker Campbell, Yesha Patel, Tara L. Moore, Maria Medalla and Ella Zeldich
Int. J. Mol. Sci. 2023, 24(4), 3477; https://doi.org/10.3390/ijms24043477 - 9 Feb 2023
Cited by 2 | Viewed by 2321
Abstract
Down syndrome (DS), or trisomy 21, is manifested in a variety of anatomical and cellular abnormalities resulting in intellectual deficits and early onset of Alzheimer’s disease (AD) with no effective treatments available to alleviate the pathologies associated with the disorder. The therapeutic potential [...] Read more.
Down syndrome (DS), or trisomy 21, is manifested in a variety of anatomical and cellular abnormalities resulting in intellectual deficits and early onset of Alzheimer’s disease (AD) with no effective treatments available to alleviate the pathologies associated with the disorder. The therapeutic potential of extracellular vesicles (EVs) has emerged recently in relation to various neurological conditions. We have previously demonstrated the therapeutic efficacy of mesenchymal stromal cell-derived EVs (MSC-EVs) in cellular and functional recovery in a rhesus monkey model of cortical injury. In the current study, we evaluated the therapeutic effect of MSC-EVs in a cortical spheroid (CS) model of DS generated from patient-derived induced pluripotent stem cells (iPSCs). Compared to euploid controls, trisomic CS display smaller size, deficient neurogenesis, and AD-related pathological features, such as enhanced cell death and depositions of amyloid beta (Aβ) and hyperphosphorylated tau (p-tau). EV-treated trisomic CS demonstrated preserved size, partial rescue in the production of neurons, significantly decreased levels of Aβ and p-tau, and a reduction in the extent of cell death as compared to the untreated trisomic CS. Together, these results show the efficacy of EVs in mitigating DS and AD-related cellular phenotypes and pathological depositions in human CS. Full article
(This article belongs to the Special Issue Therapeutic Mechanisms of Stem Cells and Exosomes for Geriatric Disease)
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15 pages, 2226 KiB  
Article
The Neuroprotective Effects of Exosomes Derived from TSG101-Overexpressing Human Neural Stem Cells in a Stroke Model
by Eun-Jung Yoon, Yunseo Choi, Tae Myoung Kim, Ehn-Kyoung Choi, Yun-Bae Kim and Dongsun Park
Int. J. Mol. Sci. 2022, 23(17), 9532; https://doi.org/10.3390/ijms23179532 - 23 Aug 2022
Cited by 13 | Viewed by 3287
Abstract
Although tissue-type plasminogen activator was approved by the FDA for early reperfusion of occluded vessels, there is a need for an effective neuroprotective drug for stroke patients. In this study, we established tumor susceptibility gene (TSG)101-overexpressing human neural stem cells (F3.TSG) and investigated [...] Read more.
Although tissue-type plasminogen activator was approved by the FDA for early reperfusion of occluded vessels, there is a need for an effective neuroprotective drug for stroke patients. In this study, we established tumor susceptibility gene (TSG)101-overexpressing human neural stem cells (F3.TSG) and investigated whether they showed enhanced secretion of exosomes and whether treatment with exosomes during reperfusion alleviated ischemia-reperfusion-mediated brain damage. F3.TSG cells secreted higher amounts of exosomes than the parental F3 cells. In N2A cells subjected to oxygen–glucose deprivation (OGD), treatment with exosomes or coculture with F3.TSG cells significantly attenuated lactate dehydrogenase release, the mRNA expression of proinflammatory factors, and the protein expression of DNA-damage-related proteins. In a middle cerebral artery occlusion (MCAO) rat model, treatment with exosomes, F3 cells, or F3.TSG cells after 2 h of occlusion followed by reperfusion reduced the infarction volume and suppressed inflammatory cytokines, DNA-damage-related proteins, and glial fibrillary acidic protein, and upregulated several neurotrophic factors. Thus, TSG101-overexpressing neural stem cells showed enhanced exosome secretion; exosome treatment protected against MCAO-induced brain damage via anti-inflammatory activities, DNA damage pathway inhibition, and growth/trophic factor induction. Therefore, exosomes and F3.TSG cells can affect neuroprotection and functional recovery in acute stroke patients. Full article
(This article belongs to the Special Issue Therapeutic Mechanisms of Stem Cells and Exosomes for Geriatric Disease)
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