AI Article Synopsis
- MicroRNAs, particularly miR-30b-5p, play a crucial role in regulating cardiac hypertrophy and the signaling marker CaMKIIδ, although the details of their integration into this process are still under investigation.
- This study identified miR-30b-5p as a significant regulator of CaMKIIδ, showing that its expression is notably reduced in hypertrophic models, indicating its potential suppressive role in cardiac hypertrophy.
- Experiments revealed that increasing miR-30b-5p levels can inhibit CaMKIIδ expression, suggesting that restoring miR-30b-5p function could be a therapeutic strategy in managing cardiac hypertrophy.
Article Abstract
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.
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| http://dx.doi.org/10.2310/JIM.0b013e3182819ac6 | DOI Listing |
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