Sialic acid accelerates the electrophoretic velocity of injured dorsal root ganglion neurons

Autor: Chen-xu Li, Guo-ying Ma, Min-fang Guo, Ying Liu
Jazyk: angličtina
Rok vydání: 2015
Předmět:
microtubule
axon
kinesin-5
Eg5
regeneration
monastrol
molecular motor protein
aging
neurodegenerative disorders
telomere shortening
MSCs
cellular therapy
traumatic brain injury
spinal cord injuries
dual diagnosis
diagnosis
complications
rehabilitation
post-concussion syndrome
brain concussion
blood brain barrier
phage display
peptide library
nanocarrier
targeting
Schwann cells
neurite outgrowth
neuromuscular junction (NMJ)
multiple sclerosis
TGF-β/BMP-7/Smad signaling
myogenic differentiation
Trf3
tumor suppression
nerve regeneration
bone marrow mesenchymal stem cells
cerebral ischemia
tail vein injection
middle cerebral artery occlusion
cell therapy
neuroprotection
brain injury
neuroimaging
ferumoxytol
superparamagnetic iron oxide particles
human adipose-derived stem cells
intracerebral injection
magnetic resonance imaging
enhanced susceptibility-weighted angiography image
modified neurological severity scores
rats
Prussian blue staining
neural regeneration
non-invasive brain stimulation
transcranial magnetic stimulation
neurotrophic factor
brain-derived neurotrophic factor
neuroplasticity
hippocampus
cognitive function
curcumin
neurons
HIV-1 gp120 V3 loop
plasticity
HIV-associated neurocognitive disorders
output/input curve
long-term potentiation
excitatory postsynaptic potential
paired-pulse facilitation
Ca 2+
synaptosome
NSFC grants
hydrogen sulfide
cerebral ischemia/reperfusion injury
P2X 7 receptor
5-triphenyl-2H-tetrazolium chloride staining
animal model
protection
sodium hydrosulfide
immunofluorescence
NSFC grant
γ-aminobutyric acid
glial fibrillary acidic protein
glutamic acid decarboxylase
neurotoxicity
weaning
organ index
cerebrum
cortex
glutamate
p53 tumor suppressor gene family
cerebral ischemia/reperfusion
pyramidal neurons
CA1 region
delayed neuronal death
immunohistochemistry
western blotting
spinal cord injury
rapamycin
Wnt/β-catenin signaling pathway
apoptosis
caspase-3
loss of neurons
hydrogen-rich saline
reactive oxygen species
physiological saline
oxidative stress
Basso
Beattie and Bresnahan score
malondialdehyde
superoxide dismutase
calcitonin gene-related peptide
peripheral nerve injury
rabbits
sciatic nerve injury
autologous nerve repair
polylactic glycolic acid conduit
extracellular matrix gel
grafting
stress relaxation
creep
viscoelasticity
histomorphology
electrophysiology
pain sense model
dorsal root ganglion
primary sensory neuron
glycosylated membrane protein
sialic acid
cell electrophoresis
electrophoresis velocity
heat-hyperalgesia behavior
hyperalgesia
neuraminidase
Neurology. Diseases of the nervous system
RC346-429
Zdroj: Neural Regeneration Research, Vol 10, Iss 6, Pp 972-975 (2015)
Druh dokumentu: article
ISSN: 1673-5374
DOI: 10.4103/1673-5374.158364
Popis: Peripheral nerve injury has been shown to result in ectopic spontaneous discharges on soma and injured sites of sensory neurons, thereby inducing neuropathic pain. With the increase of membrane proteins on soma and injured site neurons, the negatively charged sialic acids bind to the external domains of membrane proteins, resulting in an increase of this charge. We therefore speculate that the electrophoretic velocity of injured neurons may be faster than non-injured neurons. The present study established rat models of neuropathic pain via chronic constriction injury. Results of the cell electrophoresis test revealed that the electrophoretic velocity of injured neuronal cells was faster than that of non-injured (control) cells. We then treated cells with divalent cations of Ca 2+ and organic compounds with positive charges, polylysine to counteract the negatively charged sialic acids, or neuraminidase to specifically remove sialic acids from the membrane surface of injured neurons. All three treatments significantly reduced the electrophoretic velocity of injured neuronal cells. These findings suggest that enhanced sialic acids on injured neurons may accelerate the electrophoretic velocity of injured neurons.
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