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Master's Dissertation
DOI
10.11606/D.17.2018.tde-26042018-164257
Document
Author
Full name
Vanessa Almeida Amorin
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
Ribeirão Preto, 2017
Supervisor
Committee
Zinni, Cibele Maria Prado (President)
Bendhack, Lusiane Maria
Salgado, Helio Cesar
Sanchez, Elen Rizzi
Title in Portuguese
Remodelamento das proteínas contráteis cardíacas na transição da hipertrofia compensada para falência cardíaca
Keywords in Portuguese
Hipertrofia cardíaca
Insuficiência cardíaca
Maquinaria contrátil
Proteínas contráteis
Transição de hipertrofia compensada para descompensada
Abstract in Portuguese
A sobrecarga crônica de pressão causa hipertrofia, disfunção e insuficiência cardíaca (IC). O mecanismo envolvido na transição da hipertrofia cardíaca compensada para descompensada ainda não é totalmente entendido. Evidências sugerem que modificações nas proteínas contráteis poderiam contribuir para disfunção contrátil e evolução para IC. Neste sentido, estudos mostraram mudanças na expressão das proteínas da maquinaria contrátil durante o desenvolvimento da doença cardíaca como um mecanismo inicialmente benéfico. Porém, na insuficiência cardíaca, ocorrem alterações estruturais que prejudicam a contratilidade. Contudo, não se sabe ao certo quais proteínas estariam contribuindo para a transição da hipertrofia compensada para a insuficiência cardíaca. Este estudo teve como objetivo investigar as alterações das proteínas da maquinaria contrátil na transição da hipertrofia cardíaca compensada para descompensada e correlacionar essas alterações com a função cardíaca. Ratos Wistar machos foram submetidos a estenose da aorta abdominal. Após 90d da cirurgia, foram realizados ecocardiograma, análise da pressão sanguínea e os corações foram coletados para realização do Western blot e imunofluorescência para miosina de cadeia pesada, actina sarcomérica, troponina T e troponina I. Os dados foram considerados significantes quando p<0,05. Aos 90d, 70,0±5,35% dos animais apresentaram hipertrofia cardíaca (HH) e 30,3±4,79% corações hipertrofiados+dilatados (HD). A pressão arterial média aumentou 58,2% no HH e 55,0% no HD. As? expressões? de? ?-actina sarcomérica, miosina de cadeia pesada, troponina T e I aumentaram no grupo HH. No grupo HD, a miosina de cadeia pesada e a troponina T reduziram significantemente. A função sistólica manteve-se preservada nos grupos controle e HH, porém reduzida no HD. A perda estrutural da miosina de cadeia pesada e da troponina T poderia contribuir para a insuficiência cardíaca observada nesse modelo experimental.
Title in English
Remodeling of cardiac contractile proteins in the transition from compensated hypertrophy to heart failure
Keywords in English
Cardiac hypertrophy
Contractile proteins
Heart failure
Transition from compensated to decompensated cardiac hypertrophy
Abstract in English
Hypertension causes hypertrophy, cardiac dysfunction and heart failure (HF). The mechanisms implicated in the transition from compensated to decompensated cardiac hypertrophy are not fully understood. There is considerable evidence that changes in the contractile proteins may contribute to the contractile dysfunction and progression to HF. Studies have shown changes in the expression of contractile proteins during the development of heart disease as a mechanism that is initially beneficial. However, in heart failure there is an intrinsic reduction of cross-bridges that contributes to impaired contractility. It is not known which proteins are contributing to the transition from compensated hypertrophy to heart failure. We investigated ?-sarcomeric actin, heavy chain myosin and troponins T and I in the transition from compensated to decompensated cardiac hypertrophy and correlate these alterations with cardiac function. Male Wistar rats were submitted to abdominal aorta constriction and killed at 90 days post-surgery (dps). The hearts were collected; Western blot and immunofluorescence were performed to investigate ?-sarcomeric actin, heavy chain myosin and troponins T and I. Blood pressure and cardiac systolic function were evaluated. Data were considered significant when p<0.05. At 90 dps, 70,0±5,35% presented hypertrophic hearts (HH) and 30,3±4,79% hypertrophic+dilated hearts (HD). Mean blood pressure increased 58.19% in HH and 54.96% in HD. Heavy chain myosin, troponin T, troponin I and ?-sarcomeric actin expression increased in HH. In HD, only heavy chain myosin and troponin T reduced significantly. The systolic function was the same in control and HH animals and reduced in HD. The structural loss of heavy chain myosin and troponin T could contribute to heart failure observed in this experimental model of abdominal aorta constriction.
 
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Publishing Date
2018-07-11
 
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