BACKGROUND: MicroRNAs (miRNAs) participate in the regulation of cardiac hypertrophy. However, it remains largely unknown as to how miRNAs are integrated into the hypertrophic program. Ca/calmodulin-dependent protein kinase II (CaMKII) is a hypertrophic signaling marker. It is not yet clear which miRNAs can regulate CaMKIIδ. PURPOSE: In this study, we identified which miRNAs could regulate CaMKIIδ and how to regulate CaMKIIδ. METHODS: Through computational and expression analyses, miR-30b-5p was identified as a candidate regulator of CaMKIIδ. Quantitative expression analysis of hypertrophic models demonstrated significant down-regulation of miR-30b-5p compared with control groups. Luciferase reporter assay showed that miR-30b-5p could significantly inhibit the expression of CaMKIIδ. Moreover, through gain-of-function and loss-of-function approaches, we found miR-30b-5p could negatively regulate the expression of CaMKIIδ and miR-30b-5p was a regulator of cardiac hypertrophy. CONCLUSION: Our study demonstrates that the expression of miR-30b-5p is down-regulated in cardiac hypertrophy, and restoration of its function inhibits the expression of CaMKIIδ, suggesting that miR-30b-5p may act as a hypertrophic suppressor.
BACKGROUND: MicroRNAs (miRNAs) participate in the regulation of cardiac hypertrophy. However, it remains largely unknown as to how miRNAs are integrated into the hypertrophic program. Ca/calmodulin-dependent protein kinase II (CaMKII) is a hypertrophic signaling marker. It is not yet clear which miRNAs can regulate CaMKIIδ. PURPOSE: In this study, we identified which miRNAs could regulate CaMKIIδ and how to regulate CaMKIIδ. METHODS: Through computational and expression analyses, miR-30b-5p was identified as a candidate regulator of CaMKIIδ. Quantitative expression analysis of hypertrophic models demonstrated significant down-regulation of miR-30b-5p compared with control groups. Luciferase reporter assay showed that miR-30b-5p could significantly inhibit the expression of CaMKIIδ. Moreover, through gain-of-function and loss-of-function approaches, we found miR-30b-5p could negatively regulate the expression of CaMKIIδ and miR-30b-5p was a regulator of cardiac hypertrophy. CONCLUSION: Our study demonstrates that the expression of miR-30b-5p is down-regulated in cardiac hypertrophy, and restoration of its function inhibits the expression of CaMKIIδ, suggesting that miR-30b-5p may act as a hypertrophic suppressor.
Authors: Kristen M Kokkonen-Simon; Amir Saberi; Taishi Nakamura; Mark J Ranek; Guangshuo Zhu; Djahida Bedja; Michaela Kuhn; Marc K Halushka; Dong Ik Lee; David A Kass Journal: JCI Insight Date: 2018-08-09
Authors: Omar Šerý; Ivo Paclt; Ivana Drtílková; Pavel Theiner; Marta Kopečková; Petr Zvolský; Vladimir J Balcar Journal: Behav Brain Funct Date: 2015-06-11 Impact factor: 3.759
Authors: Yong Feng Liu; Amy Spinelli; Li-Yan Sun; Miao Jiang; Diane V Singer; Roman Ginnan; Fatima Z Saddouk; Dee Van Riper; Harold A Singer Journal: Sci Rep Date: 2016-05-20 Impact factor: 4.379