Long non-coding RNA-ROR aggravates myocardial ischemia/reperfusion injury

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• RNA Biology

Background:

• Long non-coding RNAs (lncRNAs) are implicated in cardiovascular diseases.
• The specific role of lncRNA-ROR in myocardial ischemia/reperfusion (I/R) injury remains largely uncharacterized.
• Understanding the molecular mechanisms of lncRNAs in I/R injury is crucial for developing novel therapeutic interventions.

Purpose of the Study:

• To investigate the role of lncRNA-ROR in myocardial I/R injury.
• To elucidate the underlying molecular mechanisms of lncRNA-ROR in the context of hypoxia/reoxygenation (H/R) and I/R.
• To assess the potential of lncRNA-ROR as a therapeutic target for myocardial I/R injury.

Main Methods:

• Quantitative real-time PCR (qRT-PCR) to measure lncRNA-ROR expression.
• Biochemical assays to assess cell injury markers (LDH, MDA, SOD, GSH-PX).
• Cell viability assays (MTT), apoptosis analysis (flow cytometry), western blotting for apoptosis factors and signaling pathways (p38/MAPK, ERK1/2), reactive oxygen species (ROS) detection, and NADPH oxidase activity/NOX2 protein measurement.

Main Results:

• lncRNA-ROR expression was upregulated in myocardial I/R patients and H/R-treated cardiomyocytes.
• lncRNA-ROR aggravated H/R-induced myocardial injury by increasing LDH, MDA, SOD, and GSH-PX release, decreasing cell viability, and promoting apoptosis.
• lncRNA-ROR enhanced ROS production, NADPH oxidase activity, and NOX2 levels, and activated the p38/MAPK and ERK1/2 pathways.

Conclusions:

• lncRNA-ROR plays a detrimental role in myocardial I/R injury.
• lncRNA-ROR promotes injury through oxidative stress and apoptosis induction.
• lncRNA-ROR inhibition presents a potential therapeutic strategy for myocardial I/R injury.