A5085738083- Mitochondrial Function and Pathology
- Neuroscience and Neuropharmacology Research
- ATP Synthase and ATPases Research
- Metabolism and Genetic Disorders
- Ion channel regulation and function
- Ubiquitin and proteasome pathways
- Trace Elements in Health
- Genetic Neurodegenerative Diseases
- Nitric Oxide and Endothelin Effects
- Alzheimer's disease research and treatments
- Metabolomics and Mass Spectrometry Studies
- Blood Coagulation and Thrombosis Mechanisms
- Heparin-Induced Thrombocytopenia and Thrombosis
- Protein Kinase Regulation and GTPase Signaling
- Muscle Physiology and Disorders
- Biotin and Related Studies
- Photosynthetic Processes and Mechanisms
- Parkinson's Disease Mechanisms and Treatments
- Heavy Metal Exposure and Toxicity
- Infectious Encephalopathies and Encephalitis
- Adipose Tissue and Metabolism
- RNA regulation and disease
- Neurobiology and Insect Physiology Research
- Drug-Induced Ocular Toxicity
- Venomous Animal Envenomation and Studies
Simon Fraser University
2008-2024
University of Pittsburgh
2003-2006
University of British Columbia
2000-2003
Mitochondria are essential to maintain neuronal viability. In addition the generation of ATP and maintenance calcium homeostasis, effective delivery mitochondria appropriate location within neurons is also likely influence their function. this study we examined mitochondrial movement morphology in primary cultures rat forebrain using a mitochondrially targeted enhanced yellow fluorescent protein (mt-eYFP). Mt-eYFP-labeled display characteristic elongated phenotype move extensively....
Mitochondria have been identified as targets of the neurotoxic actions zinc, possibly through decreased mitochondrial energy production and increased reactive oxygen species accumulation. It has hypothesized that impairment trafficking may be a mechanism neuronal injury. Here, we report elevated intraneuronal zinc impairs trafficking. At concentrations just sufficient to cause injury, rapidly inhibited movement without altering morphology. Zinc chelation initially restored movement, but...
Morphological changes in mitochondria have been primarily attributed to fission and fusion, while the more pliable transformations of (remodeling, rounding, or stretching) largely overlooked. In this study, we quantify contributions remodeling mitochondrial morphology induced by Ca(2+) ionophore 4Br-A23187 metabolic toxin rotenone. We also examine role reactive oxygen species (ROS) regulation remodeling. agreement with our previous studies, remodeling, not fission, is primary contributor...
Abstract Nitric oxide (NO) has a number of physiological and pathophysiological effects in the nervous system. One target NO is mitochondrion, where it inhibits respiration ATP synthesis, which may contribute to NO‐mediated neuronal injury. Our recent studies suggested that impaired mitochondrial function impairs trafficking, could also Here, we studied on movement morphology primary cultures forebrain neurons using mitochondrially targeted enhanced yellow fluorescent protein. produced by...
Liberation of zinc from intracellular stores contributes to oxidant-induced neuronal injury. However, little is known regarding how endogenous oxidant systems regulate free ([Zn(2+)](i)). Here we simultaneously imaged [Ca(2+)](i) and [Zn(2+)](i) study acute changes in cultured rat forebrain neurons after glutamate receptor activation. Neurons were loaded with fura-2FF FluoZin-3 follow [Zn(2+)](i), respectively. treated (100 microM) for 10 min gave large Ca(2+) responses that did not recover...
Leber's hereditary optic neuropathy (LHON) is a visual impairment associated with mutations of mitochondrial genes encoding elements the electron transport chain. While much known about genetics LHON, cellular pathophysiology leading to retinal ganglion cell degeneration and subsequent vision loss poorly understood. The impacts G11778A mutation LHON on bioenergetics, redox balance proliferation were examined in patient-derived fibroblasts. Replacement glucose galactose culture media reveals...
Mitochondrial dynamics were examined in human dermal fibroblasts biopsied from a confirmed Leber's Hereditary Optic Neuropathy (LHON) patient with homoplasmic G11778A mutation of the mitochondrial genome. Expression did not impart any discernable difference network morphology using widefield fluorescence microscopy. However, at ultrastructural level, cells expressing this exhibited an impairment morphological plasticity when forced to utilize oxidative phosphorylation (OXPHOS) by transition...
Abstract : NMDA receptors are regulated by several different calcium‐dependent processes. To determine if the presence of intracellular calcium‐binding protein calbindin‐D 28k can influence calcium regulation receptor activity,human embryonic kidney 293 cells were co‐transfected with cDNAs for subunits and cablinding. Recordings made using nystatin perforated patch technique to preserve contents. When compared control (transfected cDNA enconding β‐galactosidase in place calbindin), calbindin...
Ischemic stroke is initiated by the lack of oxygen and glucose that are normally involved in maintaining ion gradients at presynaptic terminals. Overstimulation postsynaptic glutamate receptors induces a massive influx calcium, mitochondrial depolarization, accumulation reactive species causing neuronal death. To begin to understand cellular effects on neurons following stroke, we hypothesized protein ubiquitylation would be altered due its crucial role cell signalling labeling for...
Mitochondria may be both the source and target of oxidative stress in neurodegenerative disease. In models excitotoxicity, neuronal injury is triggered by influx calcium into neurons then mitochondria. Our studies suggest that an important consequence this movement generation ROS Studies with isolated mitochondria enhance mitochondria, especially when complex I impaired. However, these are complicated a lack specificity detection methods like Amplex Red. One feature their within neurons. We...