We observed previously that glucose deprivation induces cytotoxicity, increases the intracellular levels of hydroperoxide, and activates the stress-activated protein kinase (SEK) pathway. In this study, we hypothesized that 1-methylpropyl 2-imidazolyl disulfide (IV-2), a thioredoxin (TRX) inhibitor, augments glucose deprivation-induced cytotoxicity by promoting c-Jun N-terminal kinase (JNK) act...

Glucose is one of the most important sources of cellular nutrition and glucose deprivation induces various cellular responses. In Schizosaccharomyces pombe, zinc finger protein Rst2 is activated upon glucose deprivation, and regulates gene expression via the STREP (stress response element of Schizosaccharomyces pombe) motif. However, the activation mechanism of Rst2 is not fully understood. We ...

Leptin resistance is one of the mechanisms involved in the pathophysiology of obesity. The present study showed that glucose deprivation inhibited leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) and signal transducer and activator of transcription 5 (STAT5) in neuronal cells. Flurbiprofen reversed glucose deprivation-mediated attenuation of STAT3, bu...

The ability to fuel neurons via glycogenolysis is believed to be an important function of glia. Indeed, the slow, rather than immediate, depression of synaptic transmission in hippocampal slices during exogenous glucose deprivation suggests that intrinsic energy reservoirs help to sustain neurotransmission. It is believed that glia fuel neighboring neurons via diffusible monocarboxylates such a...

The protective effect of a L-type calcium channel blocker, nimodipine, on cell injury induced by oxygen-glucose deprivation (OGD) in PC12 cells was investigated. PC12 cells were exposed to in-vitro oxygen-glucose deprivation (30 minutes and 60 minutes respectively) in the presence or absence of nimodipine (10mM/L) in three different time schedules (pre-24h, pre-3h and concurrently). Cellular vi...

In vitro ischemia models have utilized oxygen, or oxygen and glucose deprivation to simulate ischemic neuronal injury. Combined oxygen and glucose deprivation can induce neuronal damage which is in part mediated through NMDA receptors. Severe oxygen deprivation alone however can cause neuronal injury which is not NMDA mediated. We tested the hypothesis that NMDA, or non-NMDA receptor mediated m...

BACKGROUND Cognitive impairment and brain damage in diabetes is suggested to be associated with hypoglycemia. The mechanisms of hypoglycemia-induced neural death and apoptosis are not clear and reperfusion injury may be involved. Recent studies show that glucose deprivation/reperfusion induced more neuronal cell death than glucose deprivation itself. The forkhead box O (FOXO) transcription fact...

The importin-β family members (karyopherins) mediate the majority of nucleocytoplasmic transport. Msn5 and Los1, members of the importin-β family, function in tRNA nuclear export. tRNAs move bidirectionally between the nucleus and the cytoplasm. Nuclear tRNA accumulation occurs upon amino acid (aa) or glucose deprivation. To understand the mechanisms regulating tRNA subcellular trafficking, we ...

The vasoconstrictor response of perfused rat mesenteric arteries to stimulation of sympathetic nerve fibers is markedly potentiated by glucose deprivation; this potentiation is abolished or reduced when glucose or other sugars are added. The augmentation of the vasoconstrictor response to nerve stimulation produced by glucose deprivation presumably results from an increased release of the adren...

The vasoconstrictor response of perfused rat mesenteric arteries to stimulation of sympathetic nerve fibers is markedly potentiated by glucose deprivation; this potentiation is abolished or reduced when glucose or other sugars are added. The augmentation of the vasoconstrictor response to nerve stimulation produced by glucose deprivation presumably results from an increased release of the adren...