Diabetes-induced abnormalities in ER calcium mobilization in primary and secondary nociceptive neurons

Kruglikov, Illya; Gryshchenko, O.; Shutov, Leonid P.; Kostyuk, E. P.; Kostyuk, P. G.; Voitenko, Nana

doi:10.1007/s00424-004-1263-8

Cited by 64 publications

(63 citation statements)

References 22 publications

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“…Diabetes-induced oxidative stress in sensory neurons and peripheral nerves is demonstrated by increased production of reactive oxygen species (16,22,35), lipid peroxidation (19,35), and protein nitrosylation (18). It is believed the neurodegenerative outcome is energy failure in the nerve, observed as a decrease in high energy intermediates (e.g., phosphocreatine) (17,32), impaired axonal transport of proteins (5), and suboptimal Ca 2ϩ ion pumping (8,11), and it is believed that these factors contribute to the sensory neuropathy. Because of morphological similarities with diabetic neuropathy, we have hypothesized that oxidative stress may also play a key role in degeneration of neuronal processes in rabies virus infection.…”

Section: Discussionmentioning

confidence: 99%

Role of Oxidative Stress in Rabies Virus Infection of Adult Mouse Dorsal Root Ganglion Neurons

Jackson

Kammouni

Zherebitskaya

et al. 2010

J Virol

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Rabies virus infection of dorsal root ganglia (DRG) was studied in vitro with cultured adult mouse DRG neurons. Recent in vivo studies of transgenic mice that express the yellow fluorescent protein indicate that neuronal process degeneration, involving both dendrites and axons, occurs in mice infected with the challenge virus standard (CVS) strain of rabies virus by footpad inoculation. Because of the similarities of the morphological changes in experimental rabies and in diabetic neuropathy and other diseases, we hypothesize that neuronal process degeneration occurs as a result of oxidative stress. DRG neurons were cultured from adult ICR mice. Two days after plating, they were infected with CVS. Immunostaining was evaluated with CVS-and mock-infected cultures for neuron specific ␤-tubulin, rabies virus antigen, and amino acid adducts of 4-hydroxy-2-nonenal (4-HNE) (marker of lipid peroxidation and hence oxidative stress). Neuronal viability (by trypan blue exclusion), terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining, and axonal growth were also assessed with the cultures. CVS infected 33 to 54% of cultured DRG neurons. Levels of neuronal viability and TUNEL staining were similar in CVS-and mock-infected DRG neurons. There were significantly more 4-HNE-labeled puncta at 2 and 3 days postinfection in CVS-infected cultures than in mock-infected cultures, and axonal outgrowth was reduced at these time points in CVS infection. Axonal swellings with 4-HNE-labeled puncta were also associated with aggregations of actively respiring mitochondria. We have found evidence that rabies virus infection in vitro causes axonal injury of DRG neurons through oxidative stress. Oxidative stress may be important in vivo in rabies and may explain previous observations of the degeneration of neuronal processes.Rabies is an acute viral infection of the central nervous system (CNS) that is usually fatal in humans and animals (10). Despite its lethality, under natural conditions only relatively mild histopathological lesions are typically found in association with a paucity of degenerative neuronal changes (9, 21). Li et al. (13) showed severe destruction and disorganization of axons and disruption of synaptic structures in silver-stained hippocampal sections from mice infected intracerebrally with the pathogenic N2C strain of rabies virus. Infection with the challenge virus standard (CVS) strain of rabies virus has recently been evaluated using hindlimb footpad inoculation in adult transgenic mice expressing yellow fluorescent protein (26). In this model, dendritic beading and axonal swellings were prominent, and neuronal process degeneration appeared to account for the severe clinical disease and fatal outcome. The axonal swellings exhibited striking morphological similarities to the neurodegenerative changes that occur in the axons of neurons in diabetic sensory and autonomic neuropathy and in human immunodeficiency virus (HIV) infection (4,12,24,35). Studies of cultured adult dorsal root ganglio...

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Section: Discussionmentioning

confidence: 99%

Role of Oxidative Stress in Rabies Virus Infection of Adult Mouse Dorsal Root Ganglion Neurons

Jackson

Kammouni

Zherebitskaya

et al. 2010

J Virol

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“…Protein O-GlcNAcylation is increased in both type I and type II diabetes (Hu et al, 2005). Diabetes causes a reduction in the amplitude of InsP 3 -induced Ca 2ϩ release in primary and secondary nociceptive neurons (Clark et al, 2003;Kruglikov et al, 2004). Because excessive cytosolic Ca 2ϩ is a well known mediator of neuronal death, increased O-GlcNAcylation of InsP 3 R-I leading to low channel activity would provide protection against apoptosis and associated changes in brain structure and function.…”

Section: Discussionmentioning

confidence: 99%

Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I byO-GlcNAc Glycosylation

Rengifo¹,

Gibson²,

Winkler³

et al. 2007

J. Neurosci.

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“…We also find that beta-cells from db/db mice also exhibit significant reductions in both SERCA2 and SERCA3 expression (data not shown). Moreover, SERCA function is also impaired in diabetic cardiomyocytes (39), skeletal muscle (40), smooth muscle cells (41), platelets (42), and neurons (43). Therefore, we propose that down-regulation of the SERCA pump is a hallmark of prediabetic stage.…”

Section: Discussionmentioning

confidence: 99%

Contribution of Different Mechanisms to Pancreatic Beta-cell Hyper-secretion in Non-obese Diabetic (NOD) Mice during Pre-diabetes

Zhu

Liu

et al. 2011

Journal of Biological Chemistry

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Background: Pre-diabetic islet hyper-secretion is crucial to the development of the disease but the mechanisms remain unknown. Results: We reveal dynamic changes in beta-cell mass and function in non-obese diabetic (NOD) mice of different ages. Conclusion: Beta-cell mass increase and individual beta-cell secretory ability enhancement contribute to islet hyperactivity at different stages. Significance: This may provide insights into alteration of beta-cell function during the disease progression.

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Diabetes-induced abnormalities in ER calcium mobilization in primary and secondary nociceptive neurons

Cited by 64 publications

References 22 publications

Role of Oxidative Stress in Rabies Virus Infection of Adult Mouse Dorsal Root Ganglion Neurons

Role of Oxidative Stress in Rabies Virus Infection of Adult Mouse Dorsal Root Ganglion Neurons

Regulation of the Inositol 1,4,5-Trisphosphate Receptor Type I byO-GlcNAc Glycosylation

Contribution of Different Mechanisms to Pancreatic Beta-cell Hyper-secretion in Non-obese Diabetic (NOD) Mice during Pre-diabetes

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