ArticleStem cell research & therapy2018
Autophagy is required for human umbilical cord mesenchymal stem cells to improve spatial working memory in APP/PS1 transgenic mouse model.
Article in Stem cell research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Human umbilical cord mesenchymal stem cells therapy for Alzheimer's disease: a systematic review and meta-analysis of mouse models.Frontiers in neurologyPooled it
- Perinatal Tissue-Derived Stem Cells: An Emerging Therapeutic Strategy for Challenging Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Article
- Specific mesoderm subset derived from human pluripotent stem cells ameliorates microvascular pathology in type 2 diabetic mice.Science advances · 2022Article
- Hypoxic preconditioning rejuvenates mesenchymal stem cells and enhances neuroprotection following intracerebral hemorrhage via the miR-326-mediated autophagy.Stem cell research & therapy · 2021Article
- Oxidative stress-induced RAC autophagy can improve the HUVEC functions by releasing exosomes.Journal of cellular physiology · 2020Article
- New treatment modalities in Alzheimer's disease.World journal of clinical cases · 2019Review
- Cortical interlaminar astrocytes across the therian mammal radiation.The Journal of comparative neurology · 2019Article
- Stem cell therapy in Alzheimer's disease: possible benefits and limiting drawbacks.Molecular biology reports · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent studies have shown that autophagy plays a central role in mesenchymal stem cells (MSCs), and many studies have shown that human umbilical cord MSCs (huMSCs) can treat Alzheimer's disease (AD) through a variety of mechanisms. However, no studies have looked at the effects of autophagy on neuroprotective function of huMSCs in the AD mouse model. Thus, in this study we investigated whether inhibition of autophagy could weaken or block the function of huMSCs through in vitro and in vivo experiments.
methodsIn vitro we examined huMSC migration and neuronal differentiation by inhibiting or activating autophagy; in vivo autophagy of huMSCs was inhibited by knocking down Beclin 1, and these huMSCs were transplanted into the APP/PS1 transgenic mouse. A series of related indicators were detected by T-maze task, electrophysiological experiments, immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA), and Western blotting.
resultsWe demonstrated that regulation of autophagy can affect huMSC migration and their neuronal differentiation. Moreover, inhibition of autophagy in huMSCs could not realize neuroprotective effects via anti-apoptosis or promoting neurogenesis and synapse formation compared with those of control huMSCs.
conclusionsThese findings indicate that autophagy is required for huMSCs to maintain their function and improve cognition impairment in APP/PS1 transgenic mice.
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Registered trials
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