A study of Myosin Regulatory Light Chains Phosphorylation during Mouse Heart Failure Progression

Alteration of cardiac myosin regulatory light chain (RLC) phosphorylation is often observed in cardiac diseases. Recently, studies have demonstrated how lack of RLC phosphorylation contributes to the consequence of poor cardiac muscle contraction after myocardial infarction (MI) occurs. However, nei...

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Bibliographic Details
Main Author: Lee, Victor Yuan Chen
Other Authors: Michael Ferenczi
Format: Final Year Project
Language:English
Published: 2019
Subjects:
Online Access:http://hdl.handle.net/10356/77181
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Institution: Nanyang Technological University
Language: English
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Summary:Alteration of cardiac myosin regulatory light chain (RLC) phosphorylation is often observed in cardiac diseases. Recently, studies have demonstrated how lack of RLC phosphorylation contributes to the consequence of poor cardiac muscle contraction after myocardial infarction (MI) occurs. However, neither the phosphorylation level of RLC over the course of heart failure nor the effectiveness of increasing RLC phosphorylation to rescue heart failure has been investigated. Recombinant RLC (rRLC) has been expressed and phosphorylated to 60% before being exchanged into left ventricular muscle fibres of C57BL/6 mice models of healthy and diseased states. Comparison was made between native phosphorylation levels of RLC, and between native and exchanged isometric force of cardiac muscle fibres across three different time points. Our results indicate that there is a decreasing trend in both RLC phosphorylation and isometric force of muscle fibre as heart failure progresses, and that RLC phosphorylation can be a means to rescue heart failure.