ArticlePloS one2014
Neutralization of schwann cell-secreted VEGF is protective to in vitro and in vivo experimental diabetic neuropathy.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Modeling Diabetic Neuropathy: Injury Biomarkers for Early Detection Through Neuronal and Glial In Vitro Models.International journal of molecular sciences · 2026Review
- Paeoniflorin as a candidate disease-modifying therapy for diabetic peripheral neuropathy: mechanisms, exposure challenges, and translational priorities.Frontiers in pharmacology · 2026Review
- The dual role of VEGF-A in a complex in vitro model of oxaliplatin-induced neurotoxicity: Pain-related and neuroprotective effects.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Predicting diabetic retinopathy stages using a simple nerve conduction measuring device, DPNCheckFrontiers in clinical diabetes and healthcare · 2025Article
- Article
- VEGF-A/VEGFR-1 signalling and chemotherapy-induced neuropathic pain: therapeutic potential of a novel anti-VEGFR-1 monoclonal antibody.Journal of experimental & clinical cancer research : CR · 2021Article
- Schwann cells promote prevascularization and osteogenesis of tissue-engineered bone via bone marrow mesenchymal stem cell-derived endothelial cells.Stem cell research & therapy · 2021Article
- SARS-CoV-2 spike protein co-opts VEGF-A/neuropilin-1 receptor signaling to induce analgesia.Pain · 2021Article
- The Role of c-Jun and Autocrine Signaling Loops in the Control of Repair Schwann Cells and Regeneration.Frontiers in cellular neuroscience · 2021Review
- SARS-CoV-2 Spike protein co-opts VEGF-A/Neuropilin-1 receptor signaling to induce analgesia.bioRxiv : the preprint server for biology · 2020Article
- Cortex Mori Radicis extract promotes neurite outgrowth in diabetic rats by activating PI3K/AKT signaling and inhibiting Ca2+ influx associated with the upregulation of transient receptor potential canonical channel 1.Molecular medicine reports · 2020Article
- Blocking VEGF by Bevacizumab Compromises Electrophysiological and Morphological Properties of Hippocampal Neurons.Frontiers in cellular neuroscience · 2019Article
- Painful Understanding of VEGF.Frontiers in pharmacology · 2018Article
- Schwann cell interactions with axons and microvessels in diabetic neuropathy.Nature reviews. Neurology · 2017Review
- Vascular endothelial growth factor: a neurovascular target in neurological diseases.Nature reviews. Neurology · 2016Review
- Morphological Changes of Cortical and Hippocampal Neurons after Treatment with VEGF and Bevacizumab.CNS neuroscience & therapeutics · 2016Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenetic role of vascular endothelial growth factor (VEGF) in long-term retinal and kidney complications of diabetes has been demonstrated. Conversely, little is known in diabetic neuropathy. We examined the modulation of VEGF pathway at mRNA and protein level on dorsal root ganglion (DRG) neurons and Schwann cells (SC) induced by hyperglycaemia. Moreover, we studied the effects of VEGF neutralization on hyperglycemic DRG neurons and streptozotocin-induced diabetic neuropathy. Our findings demonstrated that DRG neurons were not affected by the direct exposition to hyperglycaemia, whereas showed an impairment of neurite outgrowth ability when exposed to the medium of SC cultured in hyperglycaemia. This was mediated by an altered regulation of VEGF and FLT-1 receptors. Hyperglycaemia increased VEGF and FLT-1 mRNA without changing their intracellular protein levels in DRG neurons, decreased intracellular and secreted protein levels without changing mRNA level in SC, while reduced the expression of the soluble receptor sFLT-1 both in DRG neurons and SC. Bevacizumab, a molecule that inhibits VEGF activity preventing the interaction with its receptors, restored neurite outgrowth and normalized FLT-1 mRNA and protein levels in co-cultures. In diabetic rats, it both prevented and restored nerve conduction velocity and nociceptive thresholds. We demonstrated that hyperglycaemia early affected neurite outgrowth through the impairment of SC-derived VEGF/FLT-1 signaling and that the neutralization of SC-secreted VEGF was protective both in vitro and in vivo models of diabetic neuropathy.
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