Vascular Endothelial Growth Factor Prevents Paralysis and Motoneuron Death in a Rat Model of Excitotoxic Spinal Cord Neurodegeneration

Tovar‐y‐Romo, Luis B.; Zepeda, Angélica; Tapia, Ricardo

doi:10.1097/nen.0b013e3181567c16

Cited by 65 publications

(72 citation statements)

References 36 publications

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“…The increase in mean fluorescence intensity as well as the number of moderately immunoreactive differentiated neurons on addition of VEGF to the ALS-CSF group could also suggest restoration of cholinergic activity of the damaged neurons. Our observation was similar to that of Tovar-Y-Romo et al [20] , where VEGF rendered a protective effect on a rat model of ALS in terms of an increased number of Nissl bodies and enhanced ChAT expression. The ChAT expression also increased significantly in the NALS group suggesting a possible beneficial effect of VEGF in other diseases as well, which needs to be further evaluated.…”

Section: Vegf Supplementation Restores Chat Expressionsupporting

confidence: 79%

Vascular Endothelial Growth Factor Attenuates Neurodegenerative Changes in the NSC-34 Motor Neuron Cell Line Induced by Cerebrospinal Fluid of Sporadic Amyotrophic Lateral Sclerosis Patients

et al. 2011

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Background: Motor neuron disease or amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the selective death of motor neurons in the spinal cord as well as motor cortex. Recently, vascular endothelial growth factor (VEGF) has been identified as a neurotrophic factor in animal models of familial ALS and other neurological diseases. Objective: The present study was designed to investigate the neuroprotective role of VEGF in the more prevalent sporadic form of ALS. Methods: We studied the effect of VEGF on the NSC-34 cell line exposed to cerebrospinal fluid (CSF) from sporadic ALS patients (ALS-CSF) in terms of lactate dehydrogenase (LDH) assay as well as choline acetyltransferase (ChAT) and phosphorylated neurofilament expression by immunocytochemistry and confocal microscopy. NSC-34 cells were exposed to CSF from patients with definite ALS and compared to controls. LDH activity was assessed in the growth media, prior to and 24 h after the addition of VEGF to the cells. At similar time points, the cells were fixed and processed for immunocytochemistry to evaluate ChAT and phosphorylated neurofilament expression. Results: Exposure to ALS-CSF caused morphological changes of NSC-34 cells like reduced differentiation and aggregation of phosphorylated neurofilaments. Enhanced LDH activity and reduced ChAT immunoreactivity were also observed. Addition of VEGF to NSC-34 cells exposed to ALS-CSF was protective in terms of reduced LDH activity and restoration of ChAT expression. Conclusion: The present study confirms that VEGF exerts a neuroprotective effect on the NSC-34 cell line by attenuating the degenerative changes induced by ALS-CSF. It thus has therapeutic potential in sporadic ALS.

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Section: Vegf Supplementation Restores Chat Expressionsupporting

confidence: 79%

Vascular Endothelial Growth Factor Attenuates Neurodegenerative Changes in the NSC-34 Motor Neuron Cell Line Induced by Cerebrospinal Fluid of Sporadic Amyotrophic Lateral Sclerosis Patients

et al. 2011

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“…Recent studies indicate that VEGF also has important implications for neuronal development, function, and disease (5,14,20,26,30,31,33,(35)(36)(37). Our results suggest a novel role for target-derived VEGF in promoting and/or maintaining the sympathetic innervation of blood vessels.…”

Section: Discussionmentioning

confidence: 67%

VEGF promotes vascular sympathetic innervation

Marko

Damon²

2008

American Journal of Physiology-Heart and Circulatory Physiology

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The sympathetic nervous system, via postganglionic innervation of blood vessels and the heart, is an important determinant of cardiovascular function. The mechanisms underlying sympathetic innervation of targets are not fully understood. This study tests the hypothesis that target-derived vascular endothelial growth factor (VEGF) promotes sympathetic innervation of blood vessels. Western blot and immunohistochemical analyses indicate that VEGF is produced by vascular cells in arteries and that VEGF receptors are expressed on sympathetic nerve fibers innervating arteries. In vitro, exogenously added VEGF and VEGF produced by vascular smooth muscle cells (VSMCs) in sympathetic neurovascular cocultures inhibited semaphorin 3A (Sema3A)-induced collapse of sympathetic growth cones. In the absence of Sema3A, VEGF and VSMCs also increased growth cone area. These effects were mediated via VEGF receptor 1. In vivo, the neutralization of VEGF inhibited the reinnervation of denervated femoral arteries. These data demonstrate that target-derived VEGF plays a previously unrecognized role in promoting the growth of sympathetic axons.

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“…Additionally, VEGF-A treatment protects against AMPA-induced or ischemiainduced motoneuron degeneration in vivo (Lambrechts et al, 2003;Tovar-y-Romo et al, 2007). VEGF-A also protects against the effect of the G93A-SOD1 mutation that causes motoneuron degeneration in a mouse model of ALS (Azzouz et al, 2004).…”

Section: Vegf-a As a Survival Factor For Developing And Adult Neuronsmentioning

confidence: 99%

Diverse roles for VEGF-A in the nervous system

2012

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Vascular endothelial growth factor A (VEGF-A) is best known for its essential roles in blood vessel growth. However, evidence has emerged that VEGF-A also promotes a wide range of neuronal functions, both in vitro and in vivo, including neurogenesis, neuronal migration, neuronal survival and axon guidance. Recent studies have employed mouse models to distinguish the direct effects of VEGF on neurons from its indirect, vessel-mediated effects. Ultimately, refining our knowledge of VEGF signalling pathways in neurons should help us to understand how the current use of therapeutics targeting the VEGF pathway in cancer and eye disease might be expanded to promote neuronal health and nerve repair.

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Vascular Endothelial Growth Factor Prevents Paralysis and Motoneuron Death in a Rat Model of Excitotoxic Spinal Cord Neurodegeneration

Cited by 65 publications

References 36 publications

Vascular Endothelial Growth Factor Attenuates Neurodegenerative Changes in the NSC-34 Motor Neuron Cell Line Induced by Cerebrospinal Fluid of Sporadic Amyotrophic Lateral Sclerosis Patients

Vascular Endothelial Growth Factor Attenuates Neurodegenerative Changes in the NSC-34 Motor Neuron Cell Line Induced by Cerebrospinal Fluid of Sporadic Amyotrophic Lateral Sclerosis Patients

VEGF promotes vascular sympathetic innervation

Diverse roles for VEGF-A in the nervous system

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