Nelson 2015 Master Thesis: Difference between revisions
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{{Publication | {{Publication | ||
|title=Nelson MB (2015) The role of receptors for advanced glycation end-products (RAGE) and ceramide in cardiovascular disease. Master Thesis 1-53. | |title=Nelson MB (2015) The role of receptors for advanced glycation end-products (RAGE) and ceramide in cardiovascular disease. Master Thesis 1-53. | ||
|info=[http://scholarsarchive.byu.edu/etd/4423/] | |info=[http://scholarsarchive.byu.edu/etd/4423/] | ||
|authors=Nelson MB | |authors=Nelson MB | ||
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|journal=Master Thesis | |journal=Master Thesis | ||
|abstract=Type 2 diabetes and cigarette smoke exposure are associated with an increased risk of cardiovascular complications. The role of advanced glycation end-products (AGEs) is already well-established in numerous comorbidities including cardiomyopathy. Given the role of AGEs and their receptor, RAGE, in activating inflammatory pathways, we sought to determine whether ceramides could be a mediator of RAGE-induced altered heart mitochondrial function. Using an ''in vitro model'', we treated H9C2 cardiomyocytes with carboxy-methyl lysine-BSA, followed by mitochondrial respiration assessment. We found that mitochondrial respiration was significantly impaired in AGE-treated cells, but not when co-treated with myriocin, an inhibitor of ''de novo'' ceramide biosynthesis. Moreover, we exposed WT and RAGE KO mice to side-stream cigarette smoke and found reduced mitochondrial respiration in the left ventricle myocardium from WT mice, but the RAGE KO mice were protected from this effect. Finally, conditional over-expression of RAGE in the lungs of mice also elicited a robust increase in left ventricular ceramides. Altogether, these findings suggest a RAGE-ceramide axis as an important contributor to cardiomyopathy. | |abstract=Type 2 diabetes and cigarette smoke exposure are associated with an increased risk of cardiovascular complications. The role of advanced glycation end-products (AGEs) is already well-established in numerous comorbidities including cardiomyopathy. Given the role of AGEs and their receptor, RAGE, in activating inflammatory pathways, we sought to determine whether ceramides could be a mediator of RAGE-induced altered heart mitochondrial function. Using an ''in vitro model'', we treated H9C2 cardiomyocytes with carboxy-methyl lysine-BSA, followed by mitochondrial respiration assessment. We found that mitochondrial respiration was significantly impaired in AGE-treated cells, but not when co-treated with myriocin, an inhibitor of ''de novo'' ceramide biosynthesis. Moreover, we exposed WT and RAGE KO mice to side-stream cigarette smoke and found reduced mitochondrial respiration in the left ventricle myocardium from WT mice, but the RAGE KO mice were protected from this effect. Finally, conditional over-expression of RAGE in the lungs of mice also elicited a robust increase in left ventricular ceramides. Altogether, these findings suggest a RAGE-ceramide axis as an important contributor to cardiomyopathy. | ||
|keywords=Rat H9C2 cardiomyocyte | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Pharmacology;toxicology | ||
|organism= | |organism=Mouse, Rat | ||
|tissues=Heart | |tissues=Heart | ||
|model cell lines=Other cell lines | |model cell lines=Other cell lines | ||
|preparations=Permeabilized cells, Permeabilized tissue | |preparations=Permeabilized cells, Permeabilized tissue | ||
|diseases=Cardiovascular, Diabetes | |diseases=Cardiovascular, Diabetes | ||
|couplingstates=OXPHOS, ETS | |couplingstates=LEAK, OXPHOS, ETS | ||
|substratestates=CI, CII, CI&II | |substratestates=CI, CII, CI&II | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Revision as of 14:26, 15 July 2016
| Nelson MB (2015) The role of receptors for advanced glycation end-products (RAGE) and ceramide in cardiovascular disease. Master Thesis 1-53. |
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Nelson MB (2015) Master Thesis
Abstract: Type 2 diabetes and cigarette smoke exposure are associated with an increased risk of cardiovascular complications. The role of advanced glycation end-products (AGEs) is already well-established in numerous comorbidities including cardiomyopathy. Given the role of AGEs and their receptor, RAGE, in activating inflammatory pathways, we sought to determine whether ceramides could be a mediator of RAGE-induced altered heart mitochondrial function. Using an in vitro model, we treated H9C2 cardiomyocytes with carboxy-methyl lysine-BSA, followed by mitochondrial respiration assessment. We found that mitochondrial respiration was significantly impaired in AGE-treated cells, but not when co-treated with myriocin, an inhibitor of de novo ceramide biosynthesis. Moreover, we exposed WT and RAGE KO mice to side-stream cigarette smoke and found reduced mitochondrial respiration in the left ventricle myocardium from WT mice, but the RAGE KO mice were protected from this effect. Finally, conditional over-expression of RAGE in the lungs of mice also elicited a robust increase in left ventricular ceramides. Altogether, these findings suggest a RAGE-ceramide axis as an important contributor to cardiomyopathy. • Keywords: Rat H9C2 cardiomyocyte
Labels: MiParea: Respiration, Pharmacology;toxicology
Pathology: Cardiovascular, Diabetes
Organism: Mouse, Rat Tissue;cell: Heart Preparation: Permeabilized cells, Permeabilized tissue
Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k
