Long noncoding RNA MEG3 suppressed endothelial cell proliferation and migration through regulating miR-21

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.