Journal article

Neural suppression of miRNA-181a in the kidney elevates renin expression and exacerbates hypertension in Schlager mice

Kristy L Jackson, Cindy Gueguen, Kyungjoon Lim, Nina Eikelis, Emily R Stevenson, Fadi J Charchar, Gavin W Lambert, Sandra L Burke, Madeleine R Paterson, Francine Z Marques, Geoffrey A Head



BPH/2J mice are a genetic model of hypertension with overactivity of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS). BPH/2J display higher renal renin mRNA and low levels of its negative regulator microRNA-181a (miR-181a). We hypothesise that high renal SNS activity may reduce miR-181a expression, which contributes to elevated RAS activity and hypertension in BPH/2J. Our aim was to determine whether in vivo administration of a renal-specific miR-181a mimic or whether renal denervation could increase renal miR-181a abundance to reduce renal renin mRNA, RAS activity and hypertension in BPH/2J mice. Blood pressure (BP) in BPH/2J and normotensive BPN/3J mice was measured..

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University of Melbourne Researchers


Awarded by National Health & Medical Research Council of Australia (NHMRC)

Awarded by NHMRC/National Heart Foundation (NHF)

Awarded by NHMRC

Funding Acknowledgements

This work was supported by a grant from the National Health & Medical Research Council of Australia (NHMRC, Project grant 1065714) and in part by the Victorian Government's OIS Program. Investigators were supported by NHMRC/National Heart Foundation (NHF) Postdoctoral Fellowships (NHMRC APP1091688 to KLJ, NHMRC APP1052659 and NHF PF12M6785 and 101185 to FZM) and NHMRC Research Fellowships (APP1042492 to GWL and APP1002186 to GAH).