ArticleOncology letters2018
Upregulation of seladin-1 and nestin expression in bone marrow mesenchymal stem cell transplantation via the ERK1/2 and PI3K/Akt signaling pathways in an Alzheimer's disease model.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Design, Synthesis and Antitumor Activity Evaluation in Vitro of Novel 1,6-Naphthyridine Derivatives.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Article
- Modulation of BDNF/TrkB Signalling Pathway in Alzheimer's Disease: Mechanistic Insights and the Role of Stem Cell Therapy.Biomedicines · 2025Review
- Therapeutic potential and challenges of mesenchymal stem cells in neurological disorders: A concise analysis.Journal of neuropathology and experimental neurology · 2025Review
- Erroneous Differentiation of Tendon Stem/Progenitor Cells in the Pathogenesis of Tendinopathy: Current Evidence and Future Perspectives.Stem cell reviews and reports · 2025Review
- Bone marrow mesenchymal stem cells derived cytokines associated with AKT/IAPs signaling ameliorate Alzheimer's disease development.Stem cell research & therapy · 2025Article
- Proposed Mechanisms of Cell Therapy for Alzheimer's Disease.International journal of molecular sciences · 2024Review
- The Effect of Bone Marrow Mesenchymal Stem Cells on Nestin andIranian journal of medical sciences · 2024Article
- A combination of umbilical cord mesenchymal stem cells and monosialotetrahexosy 1 ganglioside alleviates neuroinflammation in traumatic brain injury.Experimental brain research · 2023Article
- Stem Cell Therapy for Alzheimer's Disease: A Scoping Review for 2017-2022.Biomedicines · 2023Article
- The functional mechanism of bone marrow-derived mesenchymal stem cells in the treatment of animal models with Alzheimer's disease: crosstalk between autophagy and apoptosis.Stem cell research & therapy · 2022Review
- Targeting PI3K by Natural Products: A Potential Therapeutic Strategy for Attention-deficit Hyperactivity Disorder.Current neuropharmacology · 2022Review
- Review
- Stem cell-based therapy as a promising approach in Alzheimer's disease: current perspectives on novel treatment.Cell and tissue banking · 2021Review
- Functional Mechanism of Bone Marrow-Derived Mesenchymal Stem Cells in the Treatment of Animal Models with Alzheimer's Disease: Inhibition of Neuroinflammation.Journal of inflammation research · 2021Review
- Burns Impair Blood-Brain Barrier and Mesenchymal Stem Cells Can Reverse the Process in Mice.Frontiers in immunology · 2020Article
- DHCR24 in Tumor Diagnosis and Treatment: A Comprehensive Review.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to determine the roles of bone marrow mesenchymal stem cell (BM-MSC) transplantation in a model of Alzheimer's disease (AD) and determine the underlying mechanism. The expression of selective Alzheimer's disease indicator-1 (Seladin-1) and nestin was detected using reverse transcription-quantitative polymerase chain reaction and western blot analysis. The phosphoinositide 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK)1/2 inhibitors, LY294002 and PD98059, were employed to evaluate the molecular mechanism. The results indicated that the mRNA and protein expression of Seladin-1 and nestin was lower in the AD group when compared with the control group. BM-MSC transplantation reversed this decrease in expression, potentially by increasing the protein expression of phosphorylated (p)-protein kinase B (Akt) and p-ERK1/2. In addition, LY294002 (the PI3K inhibitor) and/or PD98059 (the ERK1/2 inhibitor) blocked the enhancement of BM-MSC transplantation on the expression of Seladin-1 and nestin in the hippocampus. These results indicated that BM-MSC transplantation enhanced Seladin-1 and nestin expression potentially via a mechanism associated with the activation of the PI3K/Akt and ERK1/2 signaling pathways. The present study offers preliminary evidence that treatment with BM-MSCs may represent a potential therapeutic approach against brain lesions in AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.