Dataset Information

Catechol-modified protein extracts from human heart mitochondria after APBA chromatography

ABSTRACT: Catecholamine metabolism via monoamine oxidase (MAO) contributes to cardiac injury in models of ischemia and diabetes, but the pathogenic mechanisms involved are unclear. MAO deaminates norepinephrine (NE) and dopamine (DA) to produce H2O2 and highly reactive ‘catecholaldehydes,’ which may be toxic to mitochondria due to the localization of MAO to the outer mitochondrial membrane. We performed a comprehensive analysis of catecholamine metabolism and its impact on mitochondrial energetics in atrial myocardium obtained from patients with and without type 2 diabetes. This data set contains a list of human cardiac mitochondrial proteins that were isolated following aminophenylboronic acid (APBA) column chromatography, which allows for selective purification of catechol-modified proteins. Samples of human heart mitochondria were prepared from discarded atrial appendage biopsies taken during elective cardiac surgery. Following extraction via APBA, bands were excised from a gel and subjected to proteomics analysis.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Heart

DISEASE(S): Type 2 Diabetes Mellitus

SUBMITTER: robert Pope

LAB HEAD: Ethan J. Anderson

PROVIDER: PXD021759 | Pride | 2020-10-21

REPOSITORIES: Pride

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Publications

Enhanced Catecholamine Flux and Impaired Carbonyl Metabolism Disrupt Cardiac Mitochondrial Oxidative Phosphorylation in Diabetes Patients.

Nelson Margaret-Ann M MM Efird Jimmy T JT Kew Kimberly A KA Katunga Lalage A LA Monroe T Blake TB Doorn Jonathan A JA Beatty Cherese N CN Shi Qian Q Akhter Shahab A SA Alwair Hazaim H Robidoux Jacques J Anderson Ethan J EJ

Antioxidants & redox signaling 20201125 4

Aims: Catecholamine metabolism via monoamine oxidase (MAO) contributes to cardiac injury in models of ischemia and diabetes, but the pathogenic mechanisms involved are unclear. MAO deaminates norepinephrine (NE) and dopamine to produce H2O2 and highly reactive "catecholaldehydes," which may be toxic to mitochondria due to the localization of MAO to the outer mitochondrial membrane. We performed a comprehensive analysis of catecholamine metabolism and it ...[more]

PMID: 33066717

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Project description:DEP exposure is linked to increases in cardiovascular effects. This effect is enhanced in individuals with pre-existing disease. Animal models of cardiovascular disease are used to study this susceptibility. The heart is rich in mitochondria, which produce high levels of free radicals, leading to inactivation of tricarboxylic acid cycle enzymes. We hypothesized that a 4-wk DEP inhalation would result in strain-related structural impairment of cardiac mitochondria and changes in these enzyme activities in WKY and SHR. Male rats (12-14 wks age) were exposed whole body to air or 0.5 or 2.0 mg/m3 DEP for 6h/d, 5 d/wk for 4 wks. Neutrophilic influx was noted in the bronchoalveolar lavage fluid in both strains. A slightly lower level of baseline cardiac mitochondrial aconitase activity was seen in SHR than WKY. Aconitase activity appeared to be decreased in an exposure related manner in both strains. Significantly higher baseline levels of cardiac cytosolic ferritin and aconitase activity were seen in the SHR than WKY. No exposure-related changes were noted in either of these measures. Mitochondrial succinate and isocitrate dehydrogenase activities were not changed following DEP exposure in either strain. Transmission electron microscopy images of the heart indicated abnormalities in cardiac mitochondria of control SHR but not control WKY. No exposure related ultrastructural changes were induced by DEP in either strain. In conclusion, strain differences in cardiac biomarkers of oxidative stress and structure of mitochondria exist between SHR and WKY. DEP exposure results in small changes in cardiac mitochondrial and cytosolic markers of oxidative stress. (Abstract does not represent USEPA policy.) Experiment Overall Design: Two strains of rats (Wistar Kyoto (WKY) and spontaneously hypertensive (SH) rats were exposed to either diesel exhaust particles or clean air. Four biological replicates were used for each strain/treatment exposure. Total number of chips equals 16.

Dataset Information

Catechol-modified protein extracts from human heart mitochondria after APBA chromatography

Publications

Enhanced Catecholamine Flux and Impaired Carbonyl Metabolism Disrupt Cardiac Mitochondrial Oxidative Phosphorylation in Diabetes Patients.

Similar Datasets

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