Long noncoding RNA myocardial infarction‑associated transcript is associated with the microRNA‑150‑5p/P300 pathway in...

Area of Science:

• Cardiovascular Biology
• Molecular Cardiology
• Non-coding RNA Research

Background:

• Abnormal expression of myocardial infarction-associated transcript (MIAT) is implicated in various diseases, affecting cell proliferation, apoptosis, and migration.
• The specific role of the long non-coding RNA MIAT in regulating cardiac hypertrophy remains largely unexplored.

Purpose of the Study:

• To investigate the regulatory effect of MIAT in hypertrophic cardiomyocytes, both in vitro and in vivo.
• To elucidate the molecular mechanism underlying MIAT's involvement in cardiac hypertrophy.

Main Methods:

• Establishment of cardiac hypertrophy models using neonatal rat ventricular myocytes (NRVMs) and mice stimulated with isoproterenol (ISO).
• Assessment of MIAT expression and hypertrophy markers using echocardiography, immunofluorescence staining, western blot, and RT-qPCR.
• Evaluation of MIAT's impact on microRNA (miR)-150 and P300 expression following MIAT silencing.

Main Results:

• MIAT expression was significantly upregulated in response to ISO stimulation in both in vitro and in vivo models.
• Silencing MIAT reduced the expression of hypertrophy markers, atrial natriuretic peptide and brain natriuretic peptide, in ISO-treated NRVMs.
• MIAT knockdown led to increased miR-150 levels and decreased P300 expression in NRVMs.

Conclusions:

• MIAT acts as a positive regulator in cardiomyocyte hypertrophy.
• The MIAT/miR-150-5p axis targets P300, contributing to the development of cardiac hypertrophy.
• This axis represents a potential therapeutic target for treating heart hypertrophy.