Myocardial infarction increases ACE2 expression in rat and humans

Area of Science:

• Cardiovascular Research
• Molecular Biology
• Renin-Angiotensin System

Background:

• Angiotensin converting enzyme 2 (ACE2) is crucial for regulating angiotensin peptides.
• ACE2 deficiency is linked to impaired cardiac function and myocardial ischemia.
• Understanding ACE2 expression post-myocardial infarction (MI) is vital for cardiac injury research.

Purpose of the Study:

• To investigate the expression patterns of ACE2 in the context of myocardial infarction (MI).
• To examine the role of ACE2 in cardiac injury and its modulation of the renin-angiotensin system.
• To compare ACE2 expression in rat MI models and human failing hearts.

Main Methods:

• Quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) for gene expression analysis.
• Immunohistochemistry, activity assays, and in vitro autoradiography for protein assessment.
• Analysis of ACE and ACE2 expression in rat hearts at various time points post-MI and in human failing hearts.

Main Results:

• Both ACE and ACE2 mRNA levels significantly increased in the infarct/border zone by day 3 post-MI in rats.
• Elevated ACE and ACE2 mRNA were observed in the viable myocardium of MI rats by day 28.
• ACE2 protein was localized to macrophages, vascular endothelium, smooth muscle, and myocytes; ACE2 mRNA remained elevated despite ACE inhibition with ramipril.
• Increased ACE and ACE2 immunoreactivity was found in failing human hearts.

Conclusions:

• The upregulation of ACE2 following MI indicates its significant role in negatively modulating the renin-angiotensin system.
• ACE2 is involved in the generation and degradation of angiotensin peptides after cardiac injury.
• These findings highlight ACE2 as a potential therapeutic target in managing cardiac damage post-MI.