Lipid profile alteration of cells and exosomes in acute myocardial infarction
Autor(a) principal: | |
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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 |
Resumo: | 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. |
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Lipid profile alteration of cells and exosomes in acute myocardial infarctionBioquímica clínicaApoptoseDoenças cardiovascularesEnfarte do miocárdioCardiovascular 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.As doenças cardiovasculares são a principal causa de morte em todo o mundo. De entre estas, o enfarte do miocárdio é uma das doenças mais comuns, sendo caracterizado por isquemia que leva a morte de células cardíacas. A isquemia ocorre em consequência da privação simultânea de nutrientes e oxigénio. Enquanto a isquemia representa um dano celular, a privação de nutrientes está relacionada com efeitos cardioprotetores. A resposta das células a estes estímulos pode ser por indução de autofagia ou de apoptose, dependendo da sua capacidade de adaptação e resposta aos fatores indutores de isquemia. A autofagia é um processo auto-degradativo que permite à célula adaptar-se ao stresse e é, portanto, um processo associado à sobrevivência celular. A libertação de exossomas pelas células é também um mecanismo de adaptação cujas funções estão relacionadas com a comunicação intercelular. Por outro lado, a apoptose é um processo de morte celular programada. A regulação destes processos é de extrema importância para a sobrevivência e recuperação nos episódios de enfarte do miocárdio. Hoje em dia sabe-se que os lípidos têm um papel importante no desenvolvimento de doenças cardiovasculares embora o seu papel ainda não esteja completamente esclarecido. Os lípidos são os componentes maioritários da membrana celular e desempenham funções a nível estrutural e de sinalização. Quando exposto a diversas condições fisiopatológicas, o conteúdo lipídico das células e dos exossomas é modificado. No entanto, existem ainda poucas publicações sobre a avaliação do lipidoma de cardiomiócitos em patologias cardiovasculares. Assim, o objetivo principal deste trabalho é identificar alterações no perfil lipídico de cardiomiócitos e exossomas libertados por estes sob privação de nutrientes e de oxigénio, de forma a melhor compreender o enfarte do miocárdio e se possível identificar novos biomarcadores para esta patologia. apoptose, autofagia, biomarcadores, cardiomiócitos, doenças cardiovasculares, espectrometria de massa, exossomas, fosfolípidos, infarte do miocárdio, isquémia, lipidómica Nas células cardíacas verificamos que algumas espécies moleculares de fosfatidilcolina (PC34:1 e PC36:2), fosfatidiletanolamina (PE34:1), fosfatidilserina (PS36:1), fosfatidilinositol (PI36:2, PI38:3 e PI38:5) e esfingomielina (SM34:1) variam em isquemia e em privação de nutrientes em comparação com o controlo. Algumas variações foram específicas da privação de nutrientes como a diminuição de SM(34:1) e o aumento de PS(36:1) e outras foram específicas da isquemia como a diminuição de PC(36:2) e de LPC(16:0). A espécie molecular PC(34:1) foi a que se mostrou alterada de forma diferente em cada condição sendo que aumenta em caso de isquemia e diminui em caso da privação de nutrientes. No caso dos exossomas, os resultados obtidos permitiram verificar que houve um maior desvio entre o lipidoma de exossomas libertado em isquemia e privação de nutrientes em todas as classes de lípidos. Algumas alterações foram coincidentes com as observadas para as células, por exemplo a diminuição PC(34:1) em starvation mas outras foram diferentes. Uma vez que apenas se realizaram análises lipdómicas para uma dimensão reduzida de amostra de exossomas, serão necessários estudos futuros para a validação dos resultados obtidos. Em conclusão, a privação de nutrientes e a isquemia induzem alterações na homeostasia dos lípidos. Este trabalho sugere que os lípidos são potenciais ferramentas para avaliar se os cardiomiócitos estão a optar pela morte celular ou pela recuperação, que serão úteis para melhorar o diagnóstico e prognóstico de doenças cardiovasculares.Universidade de Aveiro2018-07-20T14:00:50Z2015-07-01T00:00:00Z2015-072017-06-24T14:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisapplication/pdfhttp://hdl.handle.net/10773/14885TID:201567474engSousa, Bebiana Costainfo:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2024-02-22T11:27:22Zoai:ria.ua.pt:10773/14885Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-20T02:50:22.412949Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Lipid profile alteration of cells and exosomes in acute myocardial infarction |
title |
Lipid profile alteration of cells and exosomes in acute myocardial infarction |
spellingShingle |
Lipid profile alteration of cells and exosomes in acute myocardial infarction Sousa, Bebiana Costa Bioquímica clínica Apoptose Doenças cardiovasculares Enfarte do miocárdio |
title_short |
Lipid profile alteration of cells and exosomes in acute myocardial infarction |
title_full |
Lipid profile alteration of cells and exosomes in acute myocardial infarction |
title_fullStr |
Lipid profile alteration of cells and exosomes in acute myocardial infarction |
title_full_unstemmed |
Lipid profile alteration of cells and exosomes in acute myocardial infarction |
title_sort |
Lipid profile alteration of cells and exosomes in acute myocardial infarction |
author |
Sousa, Bebiana Costa |
author_facet |
Sousa, Bebiana Costa |
author_role |
author |
dc.contributor.author.fl_str_mv |
Sousa, Bebiana Costa |
dc.subject.por.fl_str_mv |
Bioquímica clínica Apoptose Doenças cardiovasculares Enfarte do miocárdio |
topic |
Bioquímica clínica Apoptose Doenças cardiovasculares Enfarte do miocárdio |
description |
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. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-07-01T00:00:00Z 2015-07 2017-06-24T14:00:00Z 2018-07-20T14:00:50Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
format |
masterThesis |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10773/14885 TID:201567474 |
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http://hdl.handle.net/10773/14885 |
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TID:201567474 |
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eng |
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eng |
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info:eu-repo/semantics/openAccess |
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openAccess |
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application/pdf |
dc.publisher.none.fl_str_mv |
Universidade de Aveiro |
publisher.none.fl_str_mv |
Universidade de Aveiro |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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