Long Non-coding RNA Taurine Up-regulated Gene 1 Exacerbates Cardiac Fibrosis and Cardiomyocyte Apoptosis After Acute...

Area of Science:

• Molecular Biology
• Cardiovascular Research
• RNA Biology

Background:

• Acute myocardial infarction (AMI) involves long non-coding RNAs (lncRNAs) and microRNAs (miRNAs).
• Understanding the specific roles of lncRNAs like TUG1 in AMI pathogenesis is crucial.
• The interplay between lncRNAs, miRNAs, and target genes in cardiac injury requires further elucidation.

Purpose of the Study:

• To investigate the role of lncRNA Taurine up-regulated gene 1 (TUG1) in cardiac fibrosis and cardiomyocyte apoptosis in AMI.
• To explore the regulatory axis of TUG1, miR-27a-3p, and Zinc-finger protein 36 (ZFP36) in the context of AMI.

Main Methods:

• Established a myocardial infarction (MI) mouse model and utilized cultured HL-1 cardiomyocytes under hypoxia.
• Assessed cardiac function, myocardial pathology, fibrosis, and cardiomyocyte apoptosis.
• Analyzed cell proliferation and apoptosis following transfection with specific vectors, and validated molecular interactions.

Main Results:

• Elevated TUG1 and ZFP36, with reduced miR-27a-3p, observed in MI mice and hypoxic cells.
• Decreasing TUG1 or increasing miR-27a-3p alleviated myocardial fibrosis and cardiomyocyte apoptosis.
• TUG1 sponges miR-27a-3p, targeting ZFP36, with ZFP36 upregulation counteracting miR-27a-3p effects.

Conclusions:

• lncRNA TUG1 exacerbates cardiac fibrosis and cardiomyocyte apoptosis in AMI.
• The TUG1/miR-27a-3p/ZFP36 axis is a key pathway in AMI pathogenesis.
• Targeting TUG1 or modulating this axis may offer therapeutic strategies for AMI.