50 research outputs found
Oxidative stress participates in the breakdown of neuronal phenotype in experimental diabetic neuropathy
Population-based incidence and comparative demographics of community-associated and healthcare-associated Escherichia coli bloodstream infection in Auckland, New Zealand, 2005 – 2011
Relationship between cardiovascular dysfunction and hyperglycemia in streptozotocin-induced diabetes in rats
Antioxidants and neurotrophic support in experimental diabetes
SIGLEAvailable from British Library Document Supply Centre- DSC:DXN058920 / BLDSC - British Library Document Supply CentreGBUnited Kingdo
Oxidative stress participates in the breakdown of neuronal phenotype in experimental diabetic neuropathy
Activation of JNK in Sensory Neurons Protects against Sensory Neuron Cell Death in Diabetes and on Exposure to Glucose/Oxidative Stress in Vitro
Role for nitrosative stress in diabetic neuropathy: evidence from studies with a peroxynitrite decomposition catalyst
Aberrant neurofilament phosphorylation in sensory neurons of rats with diabetic neuropathy
Aberrant neurofilament phosphorylation occurs in many neurodegenerative diseases, and in this study, two animal models of type 1 diabetes-the spontaneously diabetic BB rat and the streptozocin-induced diabetic rat-have been used to determine whether such a phenomenon is involved in the etiology of the symmetrical sensory polyneuropathy commonly associated with diabetes. There was a two- to threefold (P <0.05) elevation of neurofilament phosphorylation in lumbar dorsal root ganglia (DRG) of diabetic rats that was localized to perikarya of medium to large neurons using immunocytochemistry. Additionally, diabetes enhanced neurofilament M phosphorylation by 2.5-fold (P <0.001) in sural nerve of BB rats. Neurofilaments are substrates of the mitogen-activated protein kinase (MAPK) family, which includes c-jun NH 2- terminal kinase (JNK) or stress-activated protein kinase (SAPK1) and extracellular signal-regulated kinases (ERKs) 1 and 2. Diabetes induced a significant three- to fourfold (P <0.05) increase in phosphorylation of a 54-kDa isoform of JNK in DRG and sural nerve, and this correlated with elevated c-Jun and neurofilament phosphorylation. In diabetes, ERK phosphorylation was also increased in the DRG, but not in sural nerve. Immunocytochemistry showed that JNK was present in sensory neuron perikarya and axons. Motoneuron perikarya and peroneal nerve of diabetic rats showed no evidence of increased neurofilament phosphorylation and failed to exhibit phosphorylation of JNK. It is hypothesized that in sensory neurons of diabetic rats, aberrant phosphorylation of neurofilament may contribute to the distal sensory axonopathy observed in diabetes