Amyloid beta-derived neuroplasticity in bone marrow-derived mesenchymal stem cells is mediated by NPY and 5-HT2B receptorsviaERK1/2 signalling pathways
| العنوان: | Amyloid beta-derived neuroplasticity in bone marrow-derived mesenchymal stem cells is mediated by NPY and 5-HT2B receptorsviaERK1/2 signalling pathways |
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| المؤلفون: | Shigeki Furuya, Jae-sung Bae, Janet Carter, Hee Kyung Jin |
| المصدر: | Cell Proliferation. 42:571-586 |
| بيانات النشر: | Wiley, 2009. |
| سنة النشر: | 2009 |
| مصطلحات موضوعية: | Dynamins, MAPK/ERK pathway, Cell Survival, MAP Kinase Signaling System, Amyloid beta, medicine.medical_treatment, Apoptosis, Bone Marrow Cells, Biology, Mice, Phosphatidylinositol 3-Kinases, Alzheimer Disease, Receptor, Serotonin, 5-HT2B, medicine, Animals, Neuropeptide Y, Protein kinase A, Cells, Cultured, Mitogen-Activated Protein Kinase 1, Amyloid beta-Peptides, Mitogen-Activated Protein Kinase 3, Neuronal Plasticity, Kinase, Mesenchymal stem cell, Cell Differentiation, Mesenchymal Stem Cells, Original Articles, Cell Biology, General Medicine, Stem-cell therapy, Mice, Mutant Strains, Peptide Fragments, Receptors, Neuropeptide Y, Cell biology, Mice, Inbred C57BL, medicine.anatomical_structure, biology.protein, Bone marrow, Stem cell, Cell Division |
| الوصف: | Objective In Alzheimer's disease, toxic soluble and insoluble forms of amyloid beta (Abeta) cause synaptic dysfunction and neuronal loss. Given its potential role in producing a toxic host microenvironment for transplanted donor stem cells, we investigated the interaction between Abeta and proliferation, survival, and differentiation of bone marrow-derived mesenchymal stem cells (BM-MSC) in culture. Materials and methods We used BM-MSC that had been isolated from mouse bone marrow and cultured, and we also assessed relevant reaction mechanisms using gene microarray, immunocytochemistry, and inhibitors of potential signalling molecules, such as mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK)1/2 and tyrosine protein kinase. Results and conclusions Interestingly, we found that treatment with aggregated (1-40 or 1-42) and oligomeric (1-42) Abeta promoted neuronal-like differentiation of BM-MSC without toxic effects. This was not dependent on soluble factors released from BM-MSC progeny nor solely on formation of Abeta fibrils. The effect of Abeta is mediated by G-protein coupled receptors, neuropeptide Y1 (NPY1R) and serotonin (5-hydroxytryptamine) receptor 2B, via phosphatidylinositol-3-OH kinase-dependent activation of the MAPK/ERK1/2. Our results lend support to the idea that reciprocal donor stem cell-host interactions may promote a regenerative response that can be exploited by epigenetic modulation of NPY/serotonergic gene expression, for stem cell therapy, in Alzheimer's disease. |
| تدمد: | 1365-2184 0960-7722 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e60c25f05b5406e564b4ba7062d1dd5eTest https://doi.org/10.1111/j.1365-2184.2009.00625.xTest |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....e60c25f05b5406e564b4ba7062d1dd5e |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 13652184 09607722 |
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