Global ETD Search

1	The Effect of Teneurin C-terminal Associated Peptide-1 (TCAP-1): Protection Against Hypoxic-stress and Regulation of Brain-derived Neurotrophic Factor (BDNF) in Immortalized Hypothalamic N38 Cells Ng, Tiffany 12 January 2011 (has links) Teneurin C-terminal associated peptide-1 (TCAP-1) is a recently characterized peptide that may act as one potential neuroprotective agent as it has been shown to regulate several stress-associated behaviours in rodents and possesses a number of protective actions on cells, however the mechanism remains unknown. Brain-derived neurotrophic factor (BDNF) is a neurotrophin recognized for mediating survival, differentiation, and proliferation. TCAP-1 may act, in part, via BDNF to provide neuroprotection via modulation of BDNF expression. The aim of this research was to further investigate the mechanism of TCAP’s neuroprotective actions. I show that TCAP-1 is neuroprotective and a potent enhancer of cell numbers under varying levels of oxygen. I also establish that TCAP-1 is able to influence neuronal behaviour by differentially regulating neurite growth. In addition, I indicate that TCAP-1 is able to regulate BDNF expression in immortalized mouse hypothalamic N38 cells, which suggests that TCAP-1’s neuroprotective mechanism may involve BDNF. Brain-derived neurotrophic factor BDNF Teneurin C-terminal associated peptide TCAP hypoxia neuroprotection teneurin proliferation neurite growth hypothalamus immortalized cells hippocampus 0317 0307
2	A Novel Pathway for Enhanced Metabolic Capacities Underlies the Neuroprotective Actions of Teneurin C-Terminal Associated Peptide (TCAP)-1 Xu, Mei 27 November 2012 (has links) Teneurin C-terminal Associated Peptide (TCAP)-1 is postulated to play a critical role in cellular defense mechanisms as it is highly neuroprotective against alkalotic and hypoxic stress. Optimization of metabolic pathways is recognized as an essential survival tactic by alleviating energy deficits and meeting the demands to cope with the stressors. The aim of this research was to delineate the mechanism through which TCAP-1 confers protection. My findings show that TCAP-1 increases the overall expression of GLUT1 and enhances overall expression and membrane localization of GLUT3. With respect to metabolic parameters, chronic TCAP-1 application led to increased intracellular [ATP] with decreased intracellular [lactate], both in a dose-dependent manner, but did not alter tumourgenic glycolytic enzyme expression or mitochondrially associated apoptotic protein expression. Contrastingly, acute TCAP-1 led to decreased intracellular [ATP]. Indicative of increased cellular ATP production and physiological energy expenditure, TCAP-1 reduced serum insulin levels and subcutaneous adipocyte size in vivo. Glucose Apoptosis Stress Neuroendocrinology Protection Metabolism ATP Lactate GLUT Adipose Leptin Insulin Glycolysis Oxidation TCAP-1 TCAP Teneurin C-terminal Associated Peptide 0379 0719 0317
3	The Effect of Teneurin C-terminal Associated Peptide-1 (TCAP-1): Protection Against Hypoxic-stress and Regulation of Brain-derived Neurotrophic Factor (BDNF) in Immortalized Hypothalamic N38 Cells Ng, Tiffany 12 January 2011 (has links) Teneurin C-terminal associated peptide-1 (TCAP-1) is a recently characterized peptide that may act as one potential neuroprotective agent as it has been shown to regulate several stress-associated behaviours in rodents and possesses a number of protective actions on cells, however the mechanism remains unknown. Brain-derived neurotrophic factor (BDNF) is a neurotrophin recognized for mediating survival, differentiation, and proliferation. TCAP-1 may act, in part, via BDNF to provide neuroprotection via modulation of BDNF expression. The aim of this research was to further investigate the mechanism of TCAP’s neuroprotective actions. I show that TCAP-1 is neuroprotective and a potent enhancer of cell numbers under varying levels of oxygen. I also establish that TCAP-1 is able to influence neuronal behaviour by differentially regulating neurite growth. In addition, I indicate that TCAP-1 is able to regulate BDNF expression in immortalized mouse hypothalamic N38 cells, which suggests that TCAP-1’s neuroprotective mechanism may involve BDNF. Brain-derived neurotrophic factor BDNF Teneurin C-terminal associated peptide TCAP hypoxia neuroprotection teneurin proliferation neurite growth hypothalamus immortalized cells hippocampus 0317 0307
4	A Novel Pathway for Enhanced Metabolic Capacities Underlies the Neuroprotective Actions of Teneurin C-Terminal Associated Peptide (TCAP)-1 Xu, Mei 27 November 2012 (has links) Teneurin C-terminal Associated Peptide (TCAP)-1 is postulated to play a critical role in cellular defense mechanisms as it is highly neuroprotective against alkalotic and hypoxic stress. Optimization of metabolic pathways is recognized as an essential survival tactic by alleviating energy deficits and meeting the demands to cope with the stressors. The aim of this research was to delineate the mechanism through which TCAP-1 confers protection. My findings show that TCAP-1 increases the overall expression of GLUT1 and enhances overall expression and membrane localization of GLUT3. With respect to metabolic parameters, chronic TCAP-1 application led to increased intracellular [ATP] with decreased intracellular [lactate], both in a dose-dependent manner, but did not alter tumourgenic glycolytic enzyme expression or mitochondrially associated apoptotic protein expression. Contrastingly, acute TCAP-1 led to decreased intracellular [ATP]. Indicative of increased cellular ATP production and physiological energy expenditure, TCAP-1 reduced serum insulin levels and subcutaneous adipocyte size in vivo. Glucose Apoptosis Stress Neuroendocrinology Protection Metabolism ATP Lactate GLUT Adipose Leptin Insulin Glycolysis Oxidation TCAP-1 TCAP Teneurin C-terminal Associated Peptide 0379 0719 0317

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