Jenny Ooi
Research Officer
Cardiac Hypertrophy
Baker Heart and Diabetes Institute
Australia
Biography
Dr Jenny Ooi is a Research Officer in the Cardiac Hypertrophy Laboratory at the Baker Heart and Diabetes Institute. Jenny was awarded her PhD from Monash University in 2013 where she studied epigenetic mechanisms (chromatin modifiers and DNA methylation) in cardiac hypertrophy with the Human Epigenetics Laboratory. In January 2013, she joined the Cardiac Hypertrophy laboratory and her project aims to further understand the role of non-coding RNAs in mice models of cardiac hypertrophy using bioinformatics and molecular approaches. The laboratory focuses on understanding the similarities and differences between physiological hypertrophy ('good' heart) and pathological hypertrophy ('bad' heart). The goal is to discover/recognize critical genes/RNAs involved in heart enlargement of the healthy heart models that are protective and to improve the function of a failing heart. With recent advances in RNA-based drugs and a microRNA based drug having successfully completed phase 2 clinical trial (Janssen et al. NEJM 2013;368:1685–94), research on small RNAs has emerged as an exciting field. The laboratory has recently demonstrated that administration of a microRNA-based drug (antimiR-34) to mice with pre-existing pathological hypertrophy and cardiac dysfunction improves cardiac function and was able to attenuate pathological remodelling (Bernardo et al. PNAS 2012 109(43):17615–20). Jenny's research project also explores the mechanism of miR-34 therapy in attenuation of cardiac hypertrophy by investigating genes and microRNAs regulated with antimiR-34 therapy.
Research Interest
Cardiac Hypertrophy
Publications
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Jenny Ooi,Vascular histone deacetylation by pharmacological HDAC inhibition Genome Research 2014;24(8):1271–84.
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Jenny Ooi,The therapeutic potential of miRNAs regulated in settings of physiological cardiac hypertrophy Future medicinal chemistry 2014;6(2):205–22.
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Jenny Ooi,Therapeutic silencing of miR-652 restores heart function and attenuates adverse remodeling in a setting of established pathological hypertrophy FASEB Journal 2014;28(12):5097–110.