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LncRNA Gm43843 Promotes Cardiac Hypertrophy via miR-153-3p/Cacna1c Axis
1Department of Cardiology, Jingzhou First Municipal Hospital, Jingzhou 434000, Hubei Province, China.
Insights
This study reveals that the long noncoding RNA Gm43843 promotes cardiac hypertrophy. Gm43843 exacerbates cardiac hypertrophy by regulating the miR-153-3p/Cacna1c axis.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Genetics
Background:
- Long noncoding RNAs (lncRNAs) are implicated in various human diseases.
- Cardiac hypertrophy, a condition of increased heart muscle mass, can lead to impaired contractility.
- The specific role of the novel lncRNA Gm43843 in cardiac hypertrophy remains largely unexplored.
Purpose of the Study:
- To investigate the function of Gm43843 in cardiac hypertrophy.
- To elucidate the molecular mechanism underlying Gm43843's role in cardiac hypertrophy.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to measure Gm43843 expression.
- Western blot assays for cardiac hypertrophy protein markers.
- Immunofluorescence (IF) assays for cellular hypertrophy evaluation.
- Mechanistic assays to determine molecular interactions.
Main Results:
- Gm43843 expression increased with higher concentrations of Angiotensin II (Ang II).
- Inhibition of Gm43843 reduced hypertrophy in mouse myocardial cells.
- The Gm43843/miR-153-3p/Cacna1c axis was identified as a key regulator of cardiac hypertrophy.
Conclusions:
- Gm43843 expression is upregulated in response to hypertrophic stimuli.
- Gm43843 plays a pro-hypertrophic role in cardiac cells.
- Targeting the Gm43843/miR-153-3p/Cacna1c pathway may offer therapeutic strategies for cardiac hypertrophy.
Abstract:
Long noncoding RNAs (lncRNAs) have been reported to engage in many human diseases, including cardiac hypertrophy. Cardiac hypertrophy was mainly caused by excessive pressure load, which can eventually lead to a decline in myocardial contractility. Gm43843, a novel lncRNA, has not been well explored in cardiac hypertrophy so far. Herein, we are going to search the function and the underlying molecular mechanism of Gm43843 in cardiac hypertrophy. Gm43843 levels were measured via qRT-PCR in mouse myocardial cells when they are treated with angiogenin II (Ang II) or transfected with different plasmids. Western blot assay was implemented to detect the cardiac hypertrophy-related protein markers, while the cell was analyzed via immunofluorescence (IF) assay to evaluate the hypertrophy. Meanwhile, the binding of Gm43843 and the putative targets was examined based on mechanistic assay results. We found that Gm43843 expression was increased with the elevated concentration of Ang II. Inhibited Gm43843 was detected to reduce the hypertrophy of mouse myocardial cells. Meanwhile, Gm43843/miR-153-3p/Cacna1c axis was found to modulate cardiac hypertrophy. In short, Gm43843 promotes cardiac hypertrophy via miR-153-3p/Cacna1c axis.
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