ArticleMolecular neurobiology2015
Role of VEGF and VEGFR2 Receptor in Reversal of ALS-CSF Induced Degeneration of NSC-34 Motor Neuron Cell Line.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Reducing CETP activity prevents memory decline in an Alzheimer's disease mouse model.EMBO molecular medicine · 2026Article
- Development of novel treatments for amyotrophic lateral sclerosis.Metabolic brain disease · 2024Review
- scAAV9-VEGF alleviates symptoms of amyotrophic lateral sclerosis (ALS) mice through regulating aromatase.Experimental brain research · 2023Article
- Oligodendroglia Confer Neuroprotection to NSC-34 Motor Neuronal Cells Against the Toxic Insults of Cerebrospinal Fluid from Sporadic Amyotrophic Lateral Sclerosis Patients.Molecular neurobiology · 2023Article
- Role of vascular endothelial growth factor as a critical neurotrophic factor for the survival and physiology of motoneurons.Neural regeneration research · 2023Review
- ALS plasma reduces the viability of NSC34 cells via altering mRNA expression of VEGF: A short report.Heliyon · 2023Article
- Neuroprotective Effect of Vascular Endothelial Growth Factor on Motoneurons of the Oculomotor System.International journal of molecular sciences · 2021Review
- Inhibition of mitochondrial complex II in neuronal cells triggers unique pathways culminating in autophagy with implications for neurodegeneration.Scientific reports · 2021Article
- 40 Years of CSF Toxicity Studies in ALS: What Have We Learnt About ALS Pathophysiology?Frontiers in molecular neuroscience · 2021Review
- Amyotrophic Lateral Sclerosis (ALS) prediction model derived from plasma and CSF biomarkers.PloS one · 2021Article
- Empty mesoporous silica particles significantly delay disease progression and extend survival in a mouse model of ALS.Scientific reports · 2020Article
- Defining novel functions for cerebrospinal fluid in ALS pathophysiology.Acta neuropathologica communications · 2020Review
- Targeted proteomic response to coffee consumption.European journal of nutrition · 2020Article
- Transmission of ALS pathogenesis by the cerebrospinal fluid.Acta neuropathologica communications · 2020Article
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- Sporadic amyotrophic lateral sclerosis (SALS) - skeletal muscle response to cerebrospinal fluid from SALS patients in a rat model.Disease models & mechanisms · 2018Article
- Etiogenic factors present in the cerebrospinal fluid from amyotrophic lateral sclerosis patients induce predominantly pro-inflammatory responses in microglia.Journal of neuroinflammation · 2017Article
- Astroglia acquires a toxic neuroinflammatory role in response to the cerebrospinal fluid from amyotrophic lateral sclerosis patients.Journal of neuroinflammation · 2016Article
- Cerebrospinal Fluid from Sporadic Amyotrophic Lateral Sclerosis Patients Induces Mitochondrial and Lysosomal Dysfunction.Neurochemical research · 2016Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial growth factor (VEGF), the well-known angiogenic factor is both neurotrophic and neuroprotective. Altered VEGF signalling is implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS), a fatal degenerative disease of motor neurons. We have shown earlier that VEGF protects NSC-34 motor neuronal cell line, when exposed to cerebrospinal fluid (CSF) from sporadic ALS patients (ALS-CSF). Here, we have investigated the consequences of ALS-CSF and VEGF supplementation on the VEGFR2 receptor and endogenous VEGF expression. ALS-CSF caused significant down-regulation of VEGFR2 as well as the Calbindin-D28K levels, but not endogenous VEGF. Exogenous supplementation restored the depletion of VEGFR2 and Calbindin-D28K with a concomitant up-regulation of endogenous VEGF. The up-regulated caspase 3 in the ALS-CSF group was reinstated to basal levels along with a significant reduction in the number of TUNEL-positive cells. Electron photomicrographs of ALS-CSF-exposed cells divulged presence of cytoplasmic vacuoles alongside severe damage to organelles like mitochondria, endoplasmic reticulum, etc. Substantial recovery of most of the damaged organelles was noted in response to VEGF supplementation. While the enhancement in endogenous VEGF levels highlights the autocrine functions, the up-regulation of VEGFR2 receptor emphasizes the paracrine functions of VEGF in modulating its neuroprotective effect against ALS-CSF. The revival of cellular organellar structure, increased calbindin expression and enhanced survival in response to VEGF supplementation consolidates the opinion that VEGF indeed has a therapeutic potential in sporadic ALS.
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