Characterization of sarcomeric protein changes during mouse heart failure progression

Cardiovascular disease, especially heart failure and its most common cause – myocardial infarction (MI), is the leading cause of morbidity and mortality. Following an MI event, the heart undergoes extensive remodelling where there is modification to the proteins especially the sarcomeric proteins re...

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Main Author: Lam, Do Thuy Uyen Ha
Other Authors: Michael Ferenczi
Format: Final Year Project
Language:English
Published: 2019
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Online Access:http://hdl.handle.net/10356/77111
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Institution: Nanyang Technological University
Language: English
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spelling sg-ntu-dr.10356-771112023-02-28T18:03:18Z Characterization of sarcomeric protein changes during mouse heart failure progression Lam, Do Thuy Uyen Ha Michael Ferenczi School of Biological Sciences DRNTU::Science::Medicine Cardiovascular disease, especially heart failure and its most common cause – myocardial infarction (MI), is the leading cause of morbidity and mortality. Following an MI event, the heart undergoes extensive remodelling where there is modification to the proteins especially the sarcomeric proteins responsible for the contractility function in cardiomyocytes. Although extensive studies have been done to elucidate the function of these proteins and their post-translational modifications (PTMs), little is known about the changes in expression and PTMs of these proteins during post- MI progression. In this study, we employed a mouse model of surgically-induced MI and two-dimensional gel electrophoresis to examine the changes in protein expression and phosphorylation level (the most prominent PTMs for sarcomeric proteins) following MI. We observed qualitatively an increase in tropomyosin dephosphorylation between day 10 and day 14 post-MI, quantitatively an elevated phosphorylation in myosin regulatory light chain at day 10 followed by its decrease to normal level at day 14. We also noticed a degradation of myosin binding protein C at both time-points. We conclude that following MI, sarcomeric proteins have their own timelines in adaptation to heart failure phenotype to maintain the myocyte contractility. It is unknown whether there is interaction between these timelines. Bachelor of Science in Biological Sciences 2019-05-08T13:43:07Z 2019-05-08T13:43:07Z 2019 Final Year Project (FYP) http://hdl.handle.net/10356/77111 en Nanyang Technological University 35 p. application/pdf
institution Nanyang Technological University
building NTU Library
continent Asia
country Singapore
Singapore
content_provider NTU Library
collection DR-NTU
language English
topic DRNTU::Science::Medicine
spellingShingle DRNTU::Science::Medicine
Lam, Do Thuy Uyen Ha
Characterization of sarcomeric protein changes during mouse heart failure progression
description Cardiovascular disease, especially heart failure and its most common cause – myocardial infarction (MI), is the leading cause of morbidity and mortality. Following an MI event, the heart undergoes extensive remodelling where there is modification to the proteins especially the sarcomeric proteins responsible for the contractility function in cardiomyocytes. Although extensive studies have been done to elucidate the function of these proteins and their post-translational modifications (PTMs), little is known about the changes in expression and PTMs of these proteins during post- MI progression. In this study, we employed a mouse model of surgically-induced MI and two-dimensional gel electrophoresis to examine the changes in protein expression and phosphorylation level (the most prominent PTMs for sarcomeric proteins) following MI. We observed qualitatively an increase in tropomyosin dephosphorylation between day 10 and day 14 post-MI, quantitatively an elevated phosphorylation in myosin regulatory light chain at day 10 followed by its decrease to normal level at day 14. We also noticed a degradation of myosin binding protein C at both time-points. We conclude that following MI, sarcomeric proteins have their own timelines in adaptation to heart failure phenotype to maintain the myocyte contractility. It is unknown whether there is interaction between these timelines.
author2 Michael Ferenczi
author_facet Michael Ferenczi
Lam, Do Thuy Uyen Ha
format Final Year Project
author Lam, Do Thuy Uyen Ha
author_sort Lam, Do Thuy Uyen Ha
title Characterization of sarcomeric protein changes during mouse heart failure progression
title_short Characterization of sarcomeric protein changes during mouse heart failure progression
title_full Characterization of sarcomeric protein changes during mouse heart failure progression
title_fullStr Characterization of sarcomeric protein changes during mouse heart failure progression
title_full_unstemmed Characterization of sarcomeric protein changes during mouse heart failure progression
title_sort characterization of sarcomeric protein changes during mouse heart failure progression
publishDate 2019
url http://hdl.handle.net/10356/77111
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