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MicroRNA-132 regulates salt-dependent steady-state renin levels in mice

Anton Jan van Zonneveld, Yu Wah Au, Wendy Stam, Sharon van Gelderen, Joris I. Rotmans, Peter M.T. Deen, Ton J. Rabelink, Roel Bijkerk

2020Communications Biology15 citationsDOIOpen Access PDF

Abstract

The body's salt and fluid balance is regulated by the renin-angiotensin-aldosterone system. Generation of prostaglandin-E2 (PGE2) in a cyclo-oxygenase-2 (COX-2)-dependent manner in the macula densa, the salt-sensing cells of the kidney, plays a dominant role in renin regulation. Here we show that miR-132 directly targets Cox-2 and affects subsequent PGE2 and renin levels. MiR-132 is induced and reduced by low- and high salt treatment, respectively, in a p38- and ERK1/2-independent and CREB- and salt inducible kinase-dependent manner. Silencing of miR-132 in mice increases macula densa COX-2 expression and elevates PGE2 and renin levels, which are abrogated by the selective COX-2-inhibitor Celecoxib. Furthermore, a low or high salt diet induces and reduces macula densa miR-132 expression, while low salt diet combined with silencing miR-132 further increases renin levels. Taken together, we demonstrate a posttranscriptional regulatory role for salt-dependent miR-132 in fine-tuning the steady-state levels of renin.

Topics & Concepts

Macula densaRenin–angiotensin systemGene silencingProstaglandin E2Internal medicineEndocrinologyChemistryAngiotensin IImicroRNACREBDownregulation and upregulationRho-associated protein kinaseProstaglandinCell biologyKinaseBiologyMedicineBiochemistryReceptorGeneBlood pressureTranscription factorMicroRNA in disease regulationCancer-related molecular mechanisms researchCircular RNAs in diseases