Lipid profile alteration of cells and exosomes in acute myocardial infarction

• Autor(a) principal: Sousa, Bebiana Costa
• Data de Publicação: 2015
• Tipo de documento: Dissertação
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10773/14885
• topic: Bioquímica clínica; Apoptose; Doenças cardiovasculares; Enfarte do miocárdio

Cardiovascular Diseases are the most significant cause of death. Myocardium infarction is one of the most common of this type of diseases and it is characterized by myocardium ischemia. Ischemia occurs in consequence of simultaneous starvation and hypoxia. While ischemia represents a cellular damage, starvation is associated with a cardioprotective effect. The cell response to this injury includes either autophagy or apoptosis depending on the ability to adapt and respond to the injury and is very important for the evolution and recovery of the myocardium infarction. Autophagy is a selfdegradative process that allows cell to adapt to stress and so it is associated with cell survival. The exosomes release by cardiomyocytes is also an adaptive process which functions are related with intercellular communication. On the other hand, apoptosis is a process of programmed cell death. It is well known that lipids play an important role in cardiovascular disease although their role is not completely understood. Lipids are the major component of a cell membrane and play structural and signaling roles. Under several physiopathological conditions, the cell and exosomes lipid content can be modified. However reports on lipidome of cardiomyocytes under cardiovascular diseases are scarce. Thus, the primary aim of this work is to identify lipid profile changes in cardiomyocytes and exosomes released by them under starvation and ischemia, in order to better understand myocardial infarction and if possible to recognize new biomarkers for myocardial infarction. Cardiac cells showed that molecular species alterations in phosphatidylcholine (PC34:1 and PC36:2), phosphatidylethanolamine (PE34:1), phosphatidylserine (PS36:1), phosphatidylinositol (PI36:2, PI38:3 and PI38:5) and sphingomyelin (SM34:1) were changed in ischemia and in starvation in comparison with control group. Some differences were specific of starvation as the decrease in SM(34:1) and the increase in PS(36:1) while apoptosis, autophagy, biomarkers, cardiomyocytes, cardiovascular diseases, exosomes, ischemia, lipidomics, mass spectrometry, myocardial infarction, phospholipids, starvation others were specific of ischemia as the decrease in PC(36:2) and LPC(16:0). The molecular specie PC(34:1) showed different alterations in each condition increasing in case of ischemia and decreasing in case of starvation. For exosomes, our results showed a deviation between the lipidome of exosomes released upon ischemia and starvation for all lipid classes. Some differences matched the ones observed in cells, for example the decrease in PC(34:1) in starvation, but others were different. Since we have only performed lipidomic analysis for a smaller sample of exosomes, it requires further studies to validate the results. In conclusion, ischemia and starvation induced changes in lipid homeostasis. Our work suggests that lipids are potential tools for evaluation of cell fate, either cell death or recovery, that will be useful to improve diagnosis and prognostic of cardiovascular diseases.