Alteration in mitochondrial Ca2+ uptake disrupts insulin signaling in hypertrophic cardiomyocytes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-12

AUTHORS

Tomás Gutiérrez, Valentina Parra, Rodrigo Troncoso, Christian Pennanen, Ariel Contreras-Ferrat, César Vasquez-Trincado, Pablo E Morales, Camila Lopez-Crisosto, Cristian Sotomayor-Flores, Mario Chiong, Beverly A Rothermel, Sergio Lavandero

ABSTRACT

BACKGROUND: Cardiac hypertrophy is characterized by alterations in both cardiac bioenergetics and insulin sensitivity. Insulin promotes glucose uptake by cardiomyocytes and its use as a substrate for glycolysis and mitochondrial oxidation in order to maintain the high cardiac energy demands. Insulin stimulates Ca(2+) release from the endoplasmic reticulum, however, how this translates to changes in mitochondrial metabolism in either healthy or hypertrophic cardiomyocytes is not fully understood. RESULTS: In the present study we investigated insulin-dependent mitochondrial Ca(2+) signaling in normal and norepinephrine or insulin like growth factor-1-induced hypertrophic cardiomyocytes. Using mitochondrion-selective Ca(2+)-fluorescent probes we showed that insulin increases mitochondrial Ca(2+) levels. This signal was inhibited by the pharmacological blockade of either the inositol 1,4,5-triphosphate receptor or the mitochondrial Ca(2+) uniporter, as well as by siRNA-dependent mitochondrial Ca(2+) uniporter knockdown. Norepinephrine-stimulated cardiomyocytes showed a significant decrease in endoplasmic reticulum-mitochondrial contacts compared to either control or insulin like growth factor-1-stimulated cells. This resulted in a reduction in mitochondrial Ca(2+) uptake, Akt activation, glucose uptake and oxygen consumption in response to insulin. Blocking mitochondrial Ca(2+) uptake was sufficient to mimic the effect of norepinephrine-induced cardiomyocyte hypertrophy on insulin signaling. CONCLUSIONS: Mitochondrial Ca(2+) uptake is a key event in insulin signaling and metabolism in cardiomyocytes. More... »

PAGES

68

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12964-014-0068-4

DOI

http://dx.doi.org/10.1186/s12964-014-0068-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1019708265

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25376904


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