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Published on: September 24, 2021
Expression of miR-133 and miR-30 in chronic atrial fibrillation in canines
1Department of Cardiology, College of Medicine, Shanghai Jiaotong University, Shanghai, People's Republic of China.
Abstract:
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. The most significant histological property of AF is atrial fibrosis, but the underlying mechanism is not clear. In this study we investigated the expression of miR-133 and miR-30, anti-fibrotic microRNAs (miRNAs), in chronic AF in canines. A total amount of 42 mongrel canines of either gender, weighing between 20 and 28 kg, were randomly assigned to the sham-operated and AF groups. All canines were subjected to weekly physical examinations and electrocardiogram. Alterations in tissue structure were assessed in atrial tissue samples by using hematoxylin and eosin and Masson's trichrome. The expression of miR-133 and miR-30 was determined by TaqMan real-time polymerase chain reaction (RT-PCR) and northern blot analyses of atrial tissue. The data were analyzed using the program SPSS 11.5 for Windows. At follow-up, rapid pacing from the left superior pulmonary vein induced sustained AF in the AF group. In the left atrium, increased interstitial fibrosis and chronic inflammation were observed. RT-PCR and northern blot analyses showed that miR-133 and miR-30 expression was downregulated in the AF group. Our results show that both miR-133 and miR-30 play an important role in controlling structural changes in chronic AF.
Insights
Atrial fibrillation (AF) is linked to atrial fibrosis. This study found that anti-fibrotic microRNAs (miRNAs) miR-133 and miR-30 were downregulated in canine AF, suggesting their role in cardiac structural changes.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Atrial fibrillation (AF) is a common cardiac arrhythmia characterized by atrial fibrosis.
- The precise mechanisms driving atrial fibrosis in AF remain unclear.
- MicroRNAs (miRNAs) like miR-133 and miR-30 are known to have anti-fibrotic properties.
Purpose of the Study:
- To investigate the expression levels of anti-fibrotic miRNAs, specifically miR-133 and miR-30, in a canine model of chronic atrial fibrillation.
- To explore the relationship between these miRNAs and the observed atrial fibrosis in AF.
Main Methods:
- A canine model of chronic atrial fibrillation was established using rapid pacing.
- Atrial tissue samples were analyzed for histological changes (hematoxylin and eosin, Masson's trichrome).
- Expression of miR-133 and miR-30 was quantified using TaqMan real-time PCR and Northern blot analysis.
Main Results:
- Sustained AF was successfully induced in the AF group, characterized by increased interstitial fibrosis and chronic inflammation in the left atrium.
- Expression levels of both miR-133 and miR-30 were significantly downregulated in the atria of canines with AF compared to controls.
- Histological analysis confirmed significant alterations in atrial tissue structure.
Conclusions:
- Downregulation of miR-133 and miR-30 is associated with atrial fibrosis in a canine model of chronic AF.
- These anti-fibrotic miRNAs likely play a crucial role in regulating structural remodeling in atrial fibrillation.
- Further research into miRNA-based therapies for AF-related fibrosis is warranted.
