Related Experiment Video
Updated: Jul 5, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Circ-MBOAT2 Regulates Angiogenesis via the miR-495/NOTCH1 Axis and Associates with Myocardial Perfusion in Patients
Wei Gao1,2, Chenguang Li1,2, Jie Yuan1,2
1Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Insights
Circular RNA MBOAT2 (circ-MBOAT2) promotes blood vessel growth via the miR-495/NOTCH1 pathway in coronary chronic total occlusion (CTO) patients. This pathway impacts myocardial perfusion improvement after revascularization.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- RNA Biology
Background:
- Coronary chronic total occlusion (CTO) revascularization outcomes are debated.
- Collateral circulation and myocardial perfusion are critical in CTO.
- Circular RNAs (circRNAs) regulate angiogenesis, but their role in CTO is unknown.
Purpose of the Study:
- To investigate the role of circ-MBOAT2 in angiogenesis in CTO patients.
- To elucidate the molecular mechanism of circ-MBOAT2 in regulating angiogenesis.
- To determine the association of circ-MBOAT2 and miR-495 with myocardial perfusion post-CTO revascularization.
Main Methods:
- High-throughput sequencing of circulating circRNAs and miRNAs in CTO and stable coronary artery disease patients.
- Verification of circ-MBOAT2 and miR-495 expression in patient cohorts.
- In vitro and in vivo studies to explore circ-MBOAT2's role in angiogenesis and the miR-495/NOTCH1 axis.
- Clinical correlation analysis with myocardial perfusion assessed by SPECT.
Main Results:
- circ-MBOAT2 was significantly upregulated, and miR-495 was downregulated in CTO patients.
- circ-MBOAT2 promoted endothelial cell tube formation and migration via the miR-495/NOTCH1 axis.
- circ-MBOAT2 and miR-495 expression levels correlated with myocardial perfusion improvement after CTO revascularization.
Conclusions:
- circ-MBOAT2 promotes angiogenesis through the miR-495/NOTCH1 pathway in CTO.
- circ-MBOAT2 and miR-495 are associated with myocardial perfusion in CTO patients.
- circ-MBOAT2 and miR-495 represent potential therapeutic targets and prognostic biomarkers for CTO.
Abstract:
Revascularization of coronary chronic total occlusion (CTO) still remains controversial. The factors that impact collateral circulation and myocardial perfusion are of interest. Circular RNA (circRNA) has been shown to regulate the process of angiogenesis. However, the effects of circ-membrane-bound O-acyltransferase domain containing 2 (circ-MBOAT2) on angiogenesis in patients with CTO were unclear. In this study, we evaluated circulating circRNAs and miRNAs in patients with CTO and stable coronary artery disease using high-throughput sequencing. Another cohort of patients were selected to verify the expressions of circ-MBOAT2 and miR-495. The role and mechanism of circ-MBOAT2 in the process of angiogenesis were explored through in vitro and vivo studies. Finally, we came back to a clinical perspective and investigated whether circ-MBOAT2 and miR-495 were associated with the improvement of myocardial perfusion evaluated by single-photon emission computed tomography (SPECT). We found that the expression of circ-MBOAT2 was significantly up-regulated while miR-495 was significantly down-regulated in patients with CTO. The expression of circ-MBOAT2 was negatively correlated with miR-495 in patients with CTO. In an in vitro study, we found that circ-MBOAT2 promoted tube formation and cell migration via the miR-495/NOTCH1 axis in endothelial cells. In an in vivo study, we showed that the inhibition of miR-495 caused the increase in collateral formation in mice after hindlimb ischemia. In a human study, we showed the expressions of circ-MBOAT2 and miR-495 were associated with myocardial perfusion improvement after revascularization of CTO. In conclusion, circ-MBOAT2 regulates angiogenesis via the miR-495/NOTCH1 axis and associates with myocardial perfusion in patients with CTO. Our findings suggest that circ-MBOAT2 and miR-495 may be potential therapeutic targets and prognostic factors for patients with CTO.
Related Concept Videos
01:24Regulation of Angiogenesis and Blood Supply
01:10Mechanism of Angiogenesis