Journal article
Therapeutic silencing of miR-652 restores heart function and attenuates adverse remodeling in a setting of established pathological hypertrophy
Bianca C Bernardo, Sally S Nguyen, Catherine E Winbanks, Xiao-Ming Gao, Esther JH Boey, Yow Keat Tham, Helen Kiriazis, Jenny YY Ooi, Enzo R Porrello, Sindhu Igoor, Colleen J Thomas, Paul Gregorevic, Ruby CY Lin, Xiao-Jun Du, Julie R McMullen
FASEB JOURNAL | FEDERATION AMER SOC EXP BIOL | Published : 2014
DOI: 10.1096/fj.14-253856
Abstract
Expression of microRNA-652 (miR-652) increases in the diseased heart, decreases in a setting of cardioprotection, and is inversely correlated with heart function. The aim of this study was to assess the therapeutic potential of inhibiting miR-652 in a mouse model with established pathological hypertrophy and cardiac dysfunction due to pressure overload. Mice were subjected to a sham operation or transverse aortic constriction (TAC) for 4 wk to induce hypertrophy and cardiac dysfunction, followed by administration of a locked nucleic acid (LNA)-antimiR-652 (miR-652 inhibitor) or LNA control. Cardiac function was assessed before and 8 wk post-treatment. Expression of miR-652 increased in heart..
View full abstractGrants
Awarded by National Health and Medical Research Council of Australia
Awarded by Australian Research Council Future Fellowship
Awarded by National Health and Medical Research Council
Awarded by National Heart Foundation
Funding Acknowledgements
This study was funded by National Health and Medical Research Council of Australia project grant 586603 (to J.R.M and R.C.Y.L), and also supported in part by the Victorian Government's Operational Infrastructure Support Program. X.J.D. and J.R.M. are National Health and Medical Research Council Senior Research Fellows (APP1043026 and 586604). J.R.M., R.C.Y.L., and P.G. are supported by an Australian Research Council Future Fellowship (FT0001657), a University of New South Wales Vice Chancellor Research Fellowship, and a R.D. Wright Biomedical Research Fellowship from the National Health and Medical Research Council (1046782), respectively. E.R.P. is supported by grants and fellowships from the National Health and Medical Research Council and the National Heart Foundation (APP1033815 and 635530). The authors declare no conflicts of interest.