ArticleMetabolic brain disease2014
Conditioned medium of human adipose-derived mesenchymal stem cells mediates protection in neurons following glutamate excitotoxicity by regulating energy metabolism and GAP-43 expression.
Article in Metabolic brain disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 76 citations in OpenAlex.
- Adipose stem cells derived extracellular vesicles alleviate retinal excitotoxicity via miR-23a-5p/PLCD1/PKCA/GluA2 axis: a potential therapeutic strategy.Stem cell research & therapy · 2026Article
- The GAP43/RAC1 axis drives glycolytic reprogramming and progression in lung adenocarcinoma.Respiratory research · 2026Article
- Current trends in exosomes as therapeutic drug delivery systems.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Extracellular vesicle therapy in neurological disorders.Journal of biomedical science · 2024Review
- Restoring Synaptic Function: How Intranasal Delivery of 3D-Cultured hUSSC Exosomes Improve Learning and Memory Deficits in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Review
- Neuroprotective and anti-inflammatory properties of proteins secreted by glial progenitor cells derived from human iPSCs.Frontiers in cellular neuroscience · 2024Article
- Unveiling the Complex Role of Exosomes in Alzheimer's Disease.Journal of inflammation research · 2024Review
- Application of emerging technologies in ischemic stroke: from clinical study to basic research.Frontiers in neurology · 2024Review
- Secretome as a Tool to Treat Neurological Conditions: Are We Ready?International journal of molecular sciences · 2023Review
- Adipose mesenchymal stem cell-derived extracellular vesicles reduce glutamate-induced excitotoxicity in the retina.Neural regeneration research · 2023Article
- HJournal of molecular neuroscience : MN · 2023Article
- Andrographolide-treated bone marrow mesenchymal stem cells-derived conditioned medium protects cardiomyocytes from injury by metabolic remodeling.Molecular biology reports · 2023Article
- Exosomes-Based Nanomedicine for Neurodegenerative Diseases: Current Insights and Future Challenges.Pharmaceutics · 2023Review
- Extracellular Vesicles in Mental Disorders: A State-of-art Review.International journal of biological sciences · 2023Review
- Extracellular vesicles and Alzheimer's disease in the novel era of Precision Medicine: implications for disease progression, diagnosis and treatment.Experimental neurology · 2022Review
- Transplantation of Nasal Olfactory Mucosa Mesenchymal Stem Cells Benefits Alzheimer's Disease.Molecular neurobiology · 2022Article
- Paracrine Effects of Mesenchymal Stem Cells in Ischemic Stroke: Opportunities and Challenges.Molecular neurobiology · 2022Review
- Generation of an Immortalized Human Adipose-Derived Mesenchymal Stromal Cell Line Suitable for Wound Healing Therapy.International journal of molecular sciences · 2022Article
- Glutamate regulates gliosis of BMSCs to promote ENS regeneration through α-KG and H3K9/H3K27 demethylation.Stem cell research & therapy · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate excitotoxicity has been implicated as one of the pathological mechanisms contributing to neuronal cell death and is involved in many neurological disorders. Stem cell transplantation is a promising approach for the treatment of nervous system damage or diseases. Previous studies have shown that mesenchymal stem cells (MSCs) have important therapeutic effects in experimental animal and preclinical disease model of central nervous system pathology. However, it is not well understood whether neurogenesis of MSCs or MSC conditioned-medium (CM) containing microparticles mediates therapeutic effects. Here, we investigated the neuroprotective effects of human adipose-derived MSCs (AMSCs) on cortical neurons using models of glutamate excitotoxicity. Following exposure to glutamate (100 μM, 15 min), cortical neurons were co-cultured with either AMSCs separated by a semiporous membrane (prohibiting direct cell-cell contact) or with AMSC-CM for 18 h. Compared to untreated control groups, AMSCs and AMSC-CM partially and similarly reduced neuronal cell damages, as indicated by reduced LDH release, a decreased number of trypan-positive cells and a decline in the number of apoptotic nuclei. Protection by CM was associated with increased GAP-43 expression and an elevated number of GAP-43-positive neurites. Furthermore, CM increased levels of ATP, NAD(+) and NADH and the ratio of NAD(+)/NADH, while preventing a glutamate-induced decline in mitochondrial membrane potential. These results demonstrate that AMSC-CM mediates direct neuroprotection by inhibiting neuronal cell damage/apoptosis, promoting nerve regeneration and repair, and restoring bioenergy following energy depletion caused by glutamate excitotoxicity.
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