Related Experiment Video
Updated: Dec 1, 2025
Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion
Published on: May 16, 2025
CDKN2B-AS1 Aggravates the Pathogenesis of Human Thoracic Aortic Dissection by Sponge to miR-320d
Xin Zhao1, Shaopeng Cheng, Shouming Li
1Department of Cardiac Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Insights
Long noncoding RNA CDKN2B-AS1 is upregulated in human thoracic aortic dissection (TAD). It promotes cell apoptosis and suppresses proliferation by sponging miR-320d, suggesting it as a therapeutic target for TAD.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- RNA Biology
Background:
- Thoracic aortic dissection (TAD) is a life-threatening cardiovascular disease with limited therapeutic options.
- The role of long noncoding RNAs (lncRNAs) in TAD pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the role and molecular mechanism of lncRNA CDKN2B-AS1 in human thoracic aortic dissection (TAD).
- To explore CDKN2B-AS1 as a potential therapeutic target for TAD.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) to assess CDKN2B-AS1 expression in human TAD tissues.
- RNA pull-down and luciferase reporter assays to elucidate interactions between CDKN2B-AS1, miR-320d, and STAT3.
- In vitro assays (CCK-8, TUNEL, Western blot) in rat aortic vascular smooth muscle cells to determine CDKN2B-AS1's biological functions.
Main Results:
- CDKN2B-AS1 expression was significantly higher in human TAD tissues compared to normal aortic tissues.
- Overexpression of CDKN2B-AS1 promoted vascular smooth muscle cell apoptosis and suppressed proliferation, while its silence had opposite effects.
- CDKN2B-AS1 functions as a molecular sponge for miR-320d, positively modulating STAT3 expression by repressing miR-320d.
Conclusions:
- CDKN2B-AS1 is dysregulated in human TAD and plays significant roles in regulating vascular smooth muscle cell behavior.
- CDKN2B-AS1 acts as a ceRNA by sponging miR-320d to upregulate STAT3, contributing to TAD.
- CDKN2B-AS1 represents a promising novel therapeutic target for human TAD.
Abstract:
In the present study, the role and molecular mechanism of long noncoding RNA CDKN2B-AS1 in human thoracic aortic dissection (TAD), a highly lethal cardiovascular disease, was investigated. The expression of CDKN2B-AS1 in human TAD and normal aortic tissues of donors were examined by quantitative real-time polymerase chain reaction. RNA pull-down assay and a series of luciferase reporter assays were performed to predict the relationships between CDKN2B-AS1, miR-320d, and STAT3. Cell counting kit 8 (CCK-8), TUNEL, and western blot assays were applied to validate the biological functions of CDKN2B-AS1 in rat aortic vascular smooth muscle cells. Results showed that CDKN2B-AS1 was expressed at a higher level in human TAD than in normal aortic tissues. CDKN2B-AS1 overexpression significantly promoted apoptosis and suppressed the proliferation of vascular smooth muscle cells. CDKN2B-AS1 silence exhibited the opposite effects. Mechanistically, CDKN2B-AS1 was identified as a molecular sponge for miR-320d and positively modulated STAT3 expression via repressing miR-320d. In conclusion, our study revealed that CDKN2B-AS1 was dysregulated and displayed multiple potential functions in human TAD. These findings suggested that CDKN2B-AS1 was a novel potential therapeutic target for human TAD.
More Related Videos
Related Concept Videos
01:26Coronary Artery Disease II: Pathophysiology
01:30Cardiomyopathy II: Dilated Cardiomyopathy