Related Experiment Video
Updated: Feb 24, 2026
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Long noncoding RNA MEG3 suppressed endothelial cell proliferation and migration through regulating miR-21
Ziheng Wu1, Yangyan He1, Donglin Li1
1Department of Vascular Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang UniversityHangzhou 310000, Zhejiang, People's Republic of China.
Abstract:
Long non-coding RNAs (lncRNAs) act critical roles in many biological processes, including cell proliferation, apoptosis, development, invasion and migration. LncRNA maternally expressed gene 3 (MEG3) is found to be downregulated in several tumors; however, its role in the atherosclerosis is still unknown. In the present study, we demonstrated that MEG3 expression level was downregulated in the coronary artery disease (CAD) tissues compared to in the control tissues. We also showed that TNF-α enhanced EC cell proliferation. In addition, the expression of MEG3 was increased in EC after treated with TNF-α. Overexpression of MEG3 suppressed EC cell proliferation and inhibited the expression of cyclin D1, ki-67 and PCNA. Elevated expression of MEG3 suppressed the type I collagen, type V collagen and proteoglycan expression. In addition, we showed that elevated expression of MEG3 suppressed the miR-21 expression in the EC and promoted the expression of RhoB and PTEN, which were the direct target genes of miR-21. We demonstrated that miR-21 expression level was upregulated in the CAD tissues compared to in the control tissues. Moreover, miR-21 expression was reversely correlated with MEG3 expression in the CAD tissues. Overexpression of MEG3 suppressed EC cell proliferation and type I collagen, type V collagen and proteoglycan expression through inhibiting miR-21 expression. These results suggested that MEG3 played a critical role in regulating EC proliferation and type I collagen, type V collagen and proteoglycan expression partly through suppressing miR-21 expression.
Insights
Long non-coding RNA MEG3 is downregulated in coronary artery disease. Upregulating MEG3 suppresses endothelial cell proliferation and extracellular matrix production by inhibiting miR-21, suggesting a therapeutic role for MEG3 in atherosclerosis.
Area of Science:
- Molecular Biology
- Genetics
- Cardiovascular Research
Background:
- Long non-coding RNAs (lncRNAs) are crucial regulators of biological processes.
- LncRNA maternally expressed gene 3 (MEG3) is implicated in various cancers but its role in atherosclerosis remains unclear.
Purpose of the Study:
- To investigate the role of MEG3 in coronary artery disease (CAD).
- To elucidate the underlying molecular mechanisms of MEG3 in regulating endothelial cell (EC) function and extracellular matrix (ECM) deposition.
Main Methods:
- Quantitative real-time PCR to assess MEG3 and miR-21 expression levels in CAD tissues and ECs.
- Cell proliferation assays (e.g., using ki-67 and PCNA) and ECM component analysis (collagens, proteoglycans).
- In vitro experiments involving MEG3 overexpression and miR-21 inhibition in ECs.
Main Results:
- MEG3 expression was significantly downregulated in CAD tissues compared to controls.
- Tumor necrosis factor-alpha (TNF-α) upregulated MEG3 expression in ECs and promoted EC proliferation.
- Overexpression of MEG3 suppressed EC proliferation, reduced cyclin D1, ki-67, and PCNA expression, and decreased collagen and proteoglycan levels.
- MEG3 overexpression inhibited miR-21 expression and consequently increased its target genes, RhoB and PTEN.
- miR-21 was upregulated in CAD tissues and inversely correlated with MEG3 expression.
Conclusions:
- MEG3 plays a protective role in atherosclerosis by suppressing EC proliferation and ECM production.
- MEG3 exerts its effects partly by inhibiting miR-21, thereby modulating downstream targets.
- MEG3 represents a potential therapeutic target for managing coronary artery disease.
Related Concept Videos
01:22MicroRNAs
01:22MicroRNAs
02:39lncRNA - Long Non-coding RNAs
02:39lncRNA - Long Non-coding RNAs
02:15Experimental RNAi
01:23RNA Interference
This process occurs naturally in cells, often through the activity of genomically-encoded microRNAs. Researchers can take advantage of this mechanism by introducing synthetic RNAs to deactivate specific genes for research or therapeutic purposes. For example, RNAi could be used...