Long noncoding RNA MEG3 deteriorates inflammatory damage by downregulating microRNA-101a.

Area of Science:

• Cardiovascular Biology
• Molecular Biology
• RNA Biology

Background:

• Valvulopathy poses a significant threat to cardiovascular health.
• Inflammatory damage is a key factor in the pathogenesis of valvulopathy.
• The role of long noncoding RNAs (lncRNAs) in cardiac inflammation is an emerging area of research.

Purpose of the Study:

• To investigate the mechanism by which lncMEG3 influences inflammatory damage in myocardial cells.
• To elucidate the relationship between lncMEG3, miR-101a, and inflammatory signaling pathways.

Main Methods:

• Cell Counting Kit-8 and flow cytometry were used to assess cell viability and apoptosis.
• Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) measured gene expression.
• Western blot and ELISA analyzed protein levels and pathway activation (JNK, NF-κB).
• Reactive oxygen species (ROS) assay quantified oxidative stress.

Main Results:

• Tumor necrosis factor-α (TNF-α) induced inflammatory damage and upregulated lncMEG3 expression.
• Overexpression of lncMEG3 exacerbated inflammatory damage and apoptosis.
• lncMEG3 negatively regulated miR-101a, and miR-101a mimic reversed lncMEG3's effects.
• lncMEG3 promoted JNK and NF-κB pathway activation by downregulating miR-101a.

Conclusions:

• lncMEG3 plays a detrimental role in cardiac inflammation.
• The lncMEG3/miR-101a axis is a critical regulator of inflammatory responses in myocardial cells.
• Targeting the lncMEG3/miR-101a interaction may offer therapeutic potential for valvulopathy.