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Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
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Ellen Dirkx obtained her PhD in 2012 in cardiac metabolism and started to work as a postdoc in Prof. Leon de Windt's laboratory.
In 2014, she obtained both an EMBO Long-term and a Marie Curie EIF fellowship in order to move to the lab of Prof. Mauro Giacca (ICGEB Trieste, Italy).
During her postdoc period she studied the role of non-coding RNA in pathological cardiac remodelling as well as cardiomyocyte proliferation.
This combined experience, and the support of an NWO-VENI fellowship, gave her the opportunity to start developing her own research line aimed at developing regenerative medicine for the heart by studying the molecular mechanisms causing the switch from cardiomyocyte hyperplasia towards hypertrophy shortly after birth.
Myocardial infarction (MI) causes cell death and triggers hypertrophic remodeling of surviving cardiomyocytes, resulting in heart failure. A therapeutic approach aiming at inducing cardiomyocyte proliferation while inhibiting the hypertrophic response would improve cardiac function and prevent MI-induced heart failure.
By bioinformatics analyses, she and her group identified the miR-106b~25 cluster, containing miR-106b, miR-93 and miR25, to potentially target a network of negative cell cycle regulators, as well as series of pro-hypertrophic factors. Based on these findings, they hypothesized that over-expression of the miR-106b~25 cluster would recover the heart muscle after MI by stimulating cardiomyocyte proliferation and inhibiting hypertrophy.
They observed that in vivo overexpression of miR-106b~25 using adeno-associated virus 9 (AAV9) in neonatal mice induced cardiomyocyte proliferation (indicated by an increased incorporation of EdU into cardiomyocytes, combined with increased levels of the proliferative markers Aurora-B and phosho-histone 3), while cardiomyocyte size was not affected.
In line with this observation, in adult mice, AAV9-miR106b~25 treatment increased heart mass without inducing hypertrophy. To test the regenerative potential of myocyte proliferation secondary to AAV9-miR-106b~25 gene transfer, mice were randomized to receive a control AAV9-MCS (empty vector) or AAV9-miR-106b~25 and sham surgery or myocardial infarction (MI). Echocardiographic measurements reported an improvement of cardiac function after MI upon AAV9-miR106b~25 treatment versus AAV9-MCS, which was associated with a reduced infarction size and a clear decrease in fibrotic damage.
In summary, this data demonstrates that AAV9-miR106b~25 treatment reduces scar formation and improves cardiac function after MI by stimulating cardiomyocyte proliferation and inhibiting hypertrophic remodelling. These findings might give rise to a new regenerative approach aiming at healing the cardiac muscle after myocardial injury.
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