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he Angiotensin II type 1 receptor (AT1R) is a key regulator of blood pressure and cardiac
contractility and it is profoundly involved in development of cardiac disease as illustrated
by the widespread use of AT1R blockers. Since several microRNAs (miRNAs) have been
implicated in cardiac disease, we asked whether miRNAs might be regulated by AT1R signals
using primary cardiac myocytes and fi
using aortas from rats with
AngII induced hypertension and isolated arteries from patients with cardiovascular disease.
rst performed global miRNA microarray analysis of angiotensin II (Ang II) mediated
miRNA regulation in HEK293N cells over-expressing the AT1R followed by verifi
quantitative PCR in HEK293N cells, cardiac myocytes and fi
ese experiments revealed
several miRNAs (miRNA-7, miRNA-29b, miRNA-129-3p, miRNA-132, and miRNA-212)
that were upregulated by Ang II. We next infused AngII in Wistar rats to investigate in vivo
regulation. All candidate miRNA?s except miR-29b were also up-regulated in rat aortas aft
chronic AngII infusion. Strongly supporting diff
erentially expressed candidate miRNA?s and
securing human relevance, we extended these fi
ndings to human arteries. Relevant candidate
miRNA?s were measured in human arteries from 16 patients treated with and 16 not treated
with AT1R blockers. Remarkably, we found a robust decrease in a set of miRNA?s including
miR-7. We are currently examining target molecules in our diff
erent experimental systems.
e perspective is that the identifi
ed miRNAs may be involved in Ang II-mediated cardiac
biology and disease. Th
is is important since modifi
ed miRNA and anti-miRNA molecules have
been reported to work directly as drugs opening novel pharmacological venues.
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