ArticleMolecular and cellular biochemistry2020
NGF mediates protection of mesenchymal stem cells-conditioned medium against 2,5-hexanedione-induced apoptosis of VSC4.1 cells via Akt/Bad pathway.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Advances in the clinical application of mesenchymal stem cells for neurological disorders.Stem cell research & therapy · 2026Review
- Bone mesenchymal stem cells attenuate axonopathy in spinal cord of rats exposed to 2,5-hexanedione via NGF-dependent and -independent pathways.Molecular and cellular biochemistry · 2026Article
- The Therapeutic Mechanisms of Mesenchymal Stem Cells in MS-A Review Focusing on Neuroprotective Properties.International journal of molecular sciences · 2024Review
- Bone marrow stromal cell-conditioned medium regenerates injured sciatic nerve by increasing expression of MPZ and NGF and decreasing apoptosis.Iranian journal of basic medical sciences · 2024Article
- Regenerative capacity of trophoblast stem cell-derived extracellular vesicles on mesenchymal stem cells.Biomaterials research · 2023Article
- Bone marrow mesenchymal stem cells promote remyelination in spinal cord by driving oligodendrocyte progenitor cell differentiation via TNFα/RelB-Hes1 pathway: a rat model study of 2,5-hexanedione-induced neurotoxicity.Stem cell research & therapy · 2021Article
- Nerve growth factor (NGF) and NGF receptors in mesenchymal stem/stromal cells: Impact on potential therapies.Stem cells translational medicine · 2021Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
It has been shown that the conditioned medium of bone mesenchymal stem cells (BMSC-CM) can inhibit apoptosis of neural cells exposed to 2,5-hexanedione (HD), but its protective mechanism remains unclear. To investigate the underlying mechanism, VSC4.1 cells were given HD and 5, 10 and 15% BMSC-CM (v/v) in the current experiment. Our data showed that BMSC-CM concentration-dependently attenuated HD-induced cell apoptosis. Moreover, BMSC-CM remarkably decreased the mitochondrial cytochrome c (Cyt C) release and the caspase-3 activity in HD-given VSC4.1 cells. Given a relatively high expression of NGF in BMSCs and BMSC-CM, we hypothesized that NGF might be an important mediator of the protection of BMSC-CM against apoptosis induced by HD. To verify our hypothesis, the VSC4.1 cells were administrated with NGF and anti-NGF antibody in addition to HD. As expected, NGF could perfectly mimic BMSC-CM's protective role and these beneficial effects were abolished by anti-NGF antibody intervention. To further explore its mechanism, inhibitors of TrkA and Akt were given to the VSC4.1 cells and NGF/Akt/Bad pathway turned out to be involved in anti-apoptotic role of BMSC-CM. Based on these findings, it was revealed that BMSC-CM beneficial role was mediated by NGF and relied on the Akt/Bad pathway.
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Registered trials
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 Socratic graph.