Increased Expression of Inactive Rhomboid Protein 2 in Circulating Monocytes after Acute Myocardial Infarction

Area of Science:

• Cardiovascular Biology
• Immunology
• Molecular Medicine

Background:

• Tumor necrosis factor-alpha (TNF-α) elevation post-acute myocardial infarction (AMI) hinders myocardial recovery.
• Inactive rhomboid protein 2 (iRhom2) facilitates TNF-α shedding via TNF-α converting enzyme (TACE).

Purpose of the Study:

• To investigate the hypothesis that iRhom2 expression elevates in circulating monocytes following AMI.
• To explore the correlation between iRhom2, inflammation markers, and left ventricular (LV) function post-AMI.

Main Methods:

• Quantitative real-time PCR was used to measure iRhom2, TACE, and TNF-α mRNA levels in monocytes from 50 AMI patients.
• Monocyte samples were collected at admission (d1) and 3 days (d3) post-AMI.
• Correlations with monocyte subsets and LV systolic function were assessed.

Main Results:

• iRhom2 mRNA expression significantly increased in monocytes from d1 to d3 post-AMI.
• TNF-α and TACE mRNA levels remained unchanged during this period.
• Elevated iRhom2 at d3 correlated positively with intermediate monocytes and serum TNF-α, and negatively with LV systolic function.

Conclusions:

• iRhom2 upregulation in monocytes post-AMI may play a role in regulating inflammation.
• iRhom2 levels are associated with LV dysfunction and cardiac remodeling after AMI.
• Modulating iRhom2 presents a potential therapeutic avenue for attenuating adverse cardiac remodeling post-AMI.