0485 : Subsarcolemmal and interfibrillar mitochondria in human atrial cardiomyocyte: an enzymatic and proteomic study in diabetic patients

Abstract

Mitochondria play a key role in cell metabolism and ATP production, but also in the regulation of cell death and notably upon episodes of myocardial ischemia-reperfusion. In a context of myocardial infarction, these injuries are increased in patients with type 2 diabetes mellitus when compared to non-diabetic patients. Whereas diabetes mellitus was shown to alter mitochondrial protein expression and metabolism in rodent experimental models, there are only few data available in human. The aim of this study was to assess the metabolism and protein expression in subsarcolemmal (SSM) and interfibrillar (IFM) mitochondria extracted from human atrial appendages in diabetic and non-diabetic patients. SSM and IFM mitochondria were isolated from human right atrial appendages in type 2 diabetes mellitus and non-diabetic patients. Electron transport chain (ETC) activities were assessed using spectrophotometric and polarographic methods. Proteomic study was performed using isobaric tags for relative and absolute quantitation (iTRAQ) labeling and matrix-assisted laser desorption/ionisation-time of flight (MALDI-TOF) mass spectrometry analysis. Differences between IFM and SSM mitochondria were observed on both ETC complexes activities and expression of mitochondrial proteins. However, functional studies on ETC did not reveal any significant difference between diabetic and non-diabetic patients in both SSM and IFM mitochondria. No difference was found between mitochondria from diabetic and nondiabetic patients using polarographic method. In addition, expression of mitochondrial proteins from both mitochondrial population (SSM and IFM) did not differ when comparing diabetic and non-diabetic patients. Our study provides no evidence for a deleterious impact of type 2 diabetes mellitus on mitochondrial ETC activity and protein expression that would explain the higher susceptibility to ischemia-reperfusion compared to non-diabetic patients. The author hereby declares no conflict of interest