MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor Agonism

Aims: To characterize the effects of long-term β-adrenergic receptor stimulation on Rem protein and mRNA expression in rat heart and possible involvement of miR-132. Methods: Adult rats were treated with isoproterenol (ISO, 150 µg.kg.h-1) for 2 d and Rem, miR-132, and α1c (the principal subunit of C...

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Main Authors: Elba D. Carrillo, Raúl Sampieri, Ascención Hernández, María C. García, Jorge A. Sánchez
Format: Article
Language:English
Published: Cell Physiol Biochem Press GmbH & Co KG 2015-04-01
Series:Cellular Physiology and Biochemistry
Subjects:
Online Access:http://www.karger.com/Article/FullText/374059
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author Elba D. Carrillo
Raúl Sampieri
Ascención Hernández
María C. García
Jorge A. Sánchez
author_facet Elba D. Carrillo
Raúl Sampieri
Ascención Hernández
María C. García
Jorge A. Sánchez
author_sort Elba D. Carrillo
collection DOAJ
description Aims: To characterize the effects of long-term β-adrenergic receptor stimulation on Rem protein and mRNA expression in rat heart and possible involvement of miR-132. Methods: Adult rats were treated with isoproterenol (ISO, 150 µg.kg.h-1) for 2 d and Rem, miR-132, and α1c (the principal subunit of Cav1.2 channels) were measured at protein and mRNA levels with western blot and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) experiments, respectively. Ca2+ currents and intracellular Ca2+ signals were evaluated in isolated cardiomyocytes. Results: Systemic administration of ISO led to decreases in Rem protein and mRNA levels (down to 49%). Furthermore, levels of the microRNAs (miRs) miR-132 and miR-214 were upregulated 5- and 9-fold, respectively. Transfection of miR-132, but not miR-214, into HEK293 cells reduced the expression of a luciferase reporter gene controlled by a conserved 3´-untranslated region (UTR) of Rem by half. Chronic ISO administration also led to a 25% decrease in the amplitude of peak L-type Ca2+ currents, a 40% decrease in α1c subunit protein abundance at the membrane level, and a 60% decrease in expression of α1c channel subunit mRNA. Conclusions: These results suggest that Rem expression is down-regulated posttranscriptionally by miR-132 in response to long-term activation of β-adrenergic signaling, but this down-regulation does not produce a larger Ca2+ influx through Cav1.2 channels.
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spelling doaj.art-5126c54a5fdb4fabbec2c2a0a40063c72022-12-21T18:48:11ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782015-04-0136114115410.1159/000374059374059MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor AgonismElba D. CarrilloRaúl SampieriAscención HernándezMaría C. GarcíaJorge A. SánchezAims: To characterize the effects of long-term β-adrenergic receptor stimulation on Rem protein and mRNA expression in rat heart and possible involvement of miR-132. Methods: Adult rats were treated with isoproterenol (ISO, 150 µg.kg.h-1) for 2 d and Rem, miR-132, and α1c (the principal subunit of Cav1.2 channels) were measured at protein and mRNA levels with western blot and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) experiments, respectively. Ca2+ currents and intracellular Ca2+ signals were evaluated in isolated cardiomyocytes. Results: Systemic administration of ISO led to decreases in Rem protein and mRNA levels (down to 49%). Furthermore, levels of the microRNAs (miRs) miR-132 and miR-214 were upregulated 5- and 9-fold, respectively. Transfection of miR-132, but not miR-214, into HEK293 cells reduced the expression of a luciferase reporter gene controlled by a conserved 3´-untranslated region (UTR) of Rem by half. Chronic ISO administration also led to a 25% decrease in the amplitude of peak L-type Ca2+ currents, a 40% decrease in α1c subunit protein abundance at the membrane level, and a 60% decrease in expression of α1c channel subunit mRNA. Conclusions: These results suggest that Rem expression is down-regulated posttranscriptionally by miR-132 in response to long-term activation of β-adrenergic signaling, but this down-regulation does not produce a larger Ca2+ influx through Cav1.2 channels.http://www.karger.com/Article/FullText/374059L-type calcium channelmiR-132miR-214RemmicroRNAsIsoproterenolα1c Subunit Cav1.2 channelL-type Ca2+ currentsCa2+ transients
spellingShingle Elba D. Carrillo
Raúl Sampieri
Ascención Hernández
María C. García
Jorge A. Sánchez
MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor Agonism
Cellular Physiology and Biochemistry
L-type calcium channel
miR-132
miR-214
Rem
microRNAs
Isoproterenol
α1c Subunit Cav1.2 channel
L-type Ca2+ currents
Ca2+ transients
title MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor Agonism
title_full MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor Agonism
title_fullStr MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor Agonism
title_full_unstemmed MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor Agonism
title_short MiR-132 Regulates Rem Expression in Cardiomyocytes During Long-Term β-Adrenoceptor Agonism
title_sort mir 132 regulates rem expression in cardiomyocytes during long term β adrenoceptor agonism
topic L-type calcium channel
miR-132
miR-214
Rem
microRNAs
Isoproterenol
α1c Subunit Cav1.2 channel
L-type Ca2+ currents
Ca2+ transients
url http://www.karger.com/Article/FullText/374059
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AT ascencionhernandez mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism
AT mariacgarcia mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism
AT jorgeasanchez mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism