LncRNA-HOTAIR Inhibits H9c2 Apoptosis After Acute Myocardial Infarction via miR-206/FN1 Axis

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• RNA Biology

Background:

• Long non-coding RNAs (lncRNAs) are implicated in acute myocardial infarction (AMI) pathogenesis.
• The precise molecular mechanisms involving lncRNAs in myocardial infarction (MI) require further elucidation.

Purpose of the Study:

• To investigate the expression and function of lncRNA HOTAIR in AMI.
• To explore the molecular mechanism of HOTAIR in regulating cardiac cell function under hypoxic conditions.

Main Methods:

• Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to assess HOTAIR expression in patient serum and a mouse model of AMI.
• In vitro studies evaluated HOTAIR's biological functions in hypoxic H9c2 cells.
• Investigated the regulatory relationship between HOTAIR, miR-206, and FN1.

Main Results:

• HOTAIR expression was significantly downregulated in the serum of AMI patients and AMI mouse models.
• Overexpression of HOTAIR enhanced H9c2 cell viability and reduced apoptosis under hypoxia.
• HOTAIR regulates cardiac cell function via the miR-206/FN1 axis, with miR-206 targeting FN1.

Conclusions:

• The HOTAIR/miR-206/FN1 signaling pathway plays a crucial role in the pathogenesis of AMI.
• Targeting the HOTAIR/miR-206/FN1 axis presents a potential therapeutic strategy for treating MI.