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Published on: April 21, 2014
MiR-1-3p that correlates with left ventricular function of HCM can serve as a potential target and differentiate HCM
Mengmeng Li1, Xiao Chen1, Liang Chen1
1State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167A Beilishi Road, Xi Cheng District, Beijing, 100037, People's Republic of China.
Insights
This study reveals unique microRNA (miRNA) expression patterns in hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). MiR-1-3p shows potential for improving cardiac function in HCM patients.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- Non-coding RNA Research
Background:
- Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are distinct heart conditions with different clinical and pathological features.
- MicroRNAs (miRNAs) are key regulators of gene expression implicated in complex diseases, including cardiomyopathies.
- Previous research has not comparatively analyzed miRNA expression profiles in the left ventricles of HCM and DCM patients.
Purpose of the Study:
- To compare the expression spectrum of specific microRNAs (miRNAs) in the left ventricles of patients with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM).
- To identify disease-specific and sensitive miRNAs in HCM and DCM.
- To investigate the correlation between specific miRNAs and cardiac function parameters in HCM.
Main Methods:
- Analysis of left ventricular heart tissue samples from 30 individuals across three groups: control, HCM, and DCM (10 samples each).
- Quantification of 13 pre-selected microRNAs (miRNAs) known to be involved in heart failure and hypertrophy.
- Validation of identified miRNA associations in a separate cohort of 17 HCM patients.
Main Results:
- MiR-155, miR-10b, and miR-23a showed elevated expression in both HCM and DCM compared to controls.
- MiR-214 was downregulated and miR-21 upregulated in DCM, but not in HCM.
- MiR-1-3p and miR-27a were differentially expressed between HCM and DCM, with downregulation observed in HCM. MiR-1-3p specifically correlated with cardiac function indicators (LVEDD, LVEF) in HCM.
Conclusions:
- Distinct cardiomyopathies exhibit unique microRNA (miRNA) expression signatures.
- MiR-1-3p and miR-27a demonstrate disease specificity and sensitivity for HCM.
- MiR-1-3p is a potential therapeutic target for improving cardiac function in end-stage HCM, with Chloride voltage-gated channel 3 (Clcn3) identified as a direct target.
Background:
MicroRNAs (miRNAs) are non-coding RNAs that function as regulators of gene expression and thereby contribute to the complex disease phenotypes. Hypertrophic cardiomyopathy (HCM) and Dilated cardiomyopathy (DCM) can cause sudden cardiac death and eventually develop into heart failure. However, they have different clinical and pathophysiological phenotype and the expressional spectrum of miRNAs in left ventricles of HCM and DCM has never been compared before.
Methods:
This study selected 30 human left ventricular heart samples belonged to three diagnostic groups (Control, HCM, DCM). Each group has ten samples. Based on previous findings, the expression of 13 different microRNAs involving heart failure and hypertrophy (miR-1-3p, miR-10b, miR-21, miR-23a, miR-27a, miR-29a, miR-133a-3p, miR-142-3p, miR-155, miR-199a-3p, miR-199a-5p, miR-214, miR-497) was measured. 17 HCM patients were included as second group to validate the associations.
Results:
We found miR-155, miR-10b and miR-23a were highly expressed in both HCM and DCM compared with control. MiR-214 was downregulated and miR-21 was upregulated in DCM but not in HCM. We also identified miR-1-3p and miR-27a expressed significantly different between HCM and DCM and both miRNAs downregulated in HCM. And only miR-1-3p correlated with left ventricular end diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) that reflected the cardiac function in HCM. A second HCM group also confirmed this correlation. We then predicted Chloride voltage-gated channel 3 (Clcn3) as a direct target gene of miR-1-3p using bioinformatics tools and confirmed it by Luciferase reporter assay.
Conclusion:
Our data demonstrated that different cardiomyopathies had unique miRNA expression pattern. And the expression levels of miR-1-3p and miR-27a had disease-specificity and sensitivity in HCM, whereas only miR-1-3p was significantly associated with left ventricular function in HCM identifying it as a potential target to improve the cardiac function in end-stage HCM. We also provide Clcn3 as a direct target of miR-1-3p which sheds light on the mechanism of HCM.
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