Angiotensin-(1-9) prevents cardiomyocyte hypertrophy by controlling mitochondrial dynamics via miR-129-3p/PKIA pathway.

Cell Death and Differentiation
Cristian Sotomayor-FloresSergio Lavandero

Abstract

Angiotensin-(1-9) is a peptide from the noncanonical renin-angiotensin system with anti-hypertrophic effects in cardiomyocytes via an unknown mechanism. In the present study we aimed to elucidate it, basing us initially on previous work from our group and colleagues who proved a relationship between disturbances in mitochondrial morphology and calcium handling, associated with the setting of cardiac hypertrophy. Our first finding was that angiotensin-(1-9) can induce mitochondrial fusion through DRP1 phosphorylation. Secondly, angiotensin-(1-9) blocked mitochondrial fission and intracellular calcium dysregulation in a model of norepinephrine-induced cardiomyocyte hypertrophy, preventing the activation of the calcineurin/NFAT signaling pathway. To further investigate angiotensin-(1-9) anti-hypertrophic mechanism, we performed RNA-seq studies, identifying the upregulation of miR-129 under angiotensin-(1-9) treatment. miR-129 decreased the transcript levels of the protein kinase A inhibitor (PKIA), resulting in the activation of the protein kinase A (PKA) signaling pathway. Finally, we showed that PKA activity is necessary for the effects of angiotensin-(1-9) over mitochondrial dynamics, calcium handling and its anti-hypertrophic ...Continue Reading

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Citations

Aug 25, 2020·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·James J HoyRamiro Iglesias-Bartolome
Oct 1, 2020·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·Ana Cristina Simões E SilvaJoseph T Flynn
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Methods Mentioned

BETA
confocal microscopy
immunoprecipitation
PCR
transfections
electrophoresis
RNA-seq
transmission electron microscopy
transfection

Software Mentioned

Quantity One
Bowtie
ImageQuant
DESeq2
Trimmomatic
TargetScan
Ensembl
BEDTools
GraphPad Prism
LSM

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