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...
Main Authors: | , , , , |
---|---|
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 |
_version_ | 1819090632405155840 |
---|---|
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. |
first_indexed | 2024-12-21T22:26:55Z |
format | Article |
id | doaj.art-5126c54a5fdb4fabbec2c2a0a40063c7 |
institution | Directory Open Access Journal |
issn | 1015-8987 1421-9778 |
language | English |
last_indexed | 2024-12-21T22:26:55Z |
publishDate | 2015-04-01 |
publisher | Cell Physiol Biochem Press GmbH & Co KG |
record_format | Article |
series | Cellular Physiology and Biochemistry |
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 |
work_keys_str_mv | AT elbadcarrillo mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism AT raulsampieri mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism AT ascencionhernandez mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism AT mariacgarcia mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism AT jorgeasanchez mir132regulatesremexpressionincardiomyocytesduringlongtermbadrenoceptoragonism |