Cardiovascular Disease

CDKN2B-AS1[LncRNA]

miR-320d[miRNA]

STAT3[mRNA]

aortic vascular smooth muscle cells

Homo sapiens (human)

J Cardiovasc Pharmacol. 2020 Nov;76(5):592-601. doi: 10.1097/FJC.0000000000000907.

CDKN2B-AS1 Aggravates the Pathogenesis of Human Thoracic Aortic Dissection by Sponge to miR-320d.

RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;

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.