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Increased Expression of Inactive Rhomboid Protein 2 in Circulating Monocytes after Acute Myocardial Infarction
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Increased Expression of Inactive Rhomboid Protein 2 in Circulating Monocytes after Acute Myocardial Infarction
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Journal Article
Increased Expression of Inactive Rhomboid Protein 2 in Circulating Monocytes after Acute Myocardial Infarction
2024
Overview
Increased TNF-α levels following acute myocardial infarction (AMI) contribute to impaired recovery of myocardial function. Interaction of inactive rhomboid protein 2 (iRhom2) with TNF-α converting enzyme (TACE) is required for TNF-α shedding from immune cells. We hypothesized that iRhom2 expression increases in circulating monocytes following AMI. Transcript levels of iRhom2, TACE and TNF-α were evaluated by quantitative real-time PCR in isolated monocytes of 50 AMI patients at admission (d1) and 3 days (d3) after. We observed a significant increase in levels of iRhom2 mRNA expression in monocytes between d1-3, while TNF-α and TACE mRNA expression remained unchanged. At d3, iRhom2 mRNA expression positively correlated with levels of intermediate monocytes or serum TNF-α, and negatively with LV systolic function. iRhom2 may contribute to regulation of post-infarction inflammation and is associated with LV dysfunction following AMI. iRhom2 modulation should be evaluated as a potential therapeutic strategy to attenuate cardiac remodeling following AMI.
Publisher
Springer US,Springer Nature B.V
Subject
/ Aged
/ Biomedical Engineering and Bioengineering
/ Carrier Proteins - metabolism
/ Female
/ Humans
/ Intracellular Signaling Peptides and Proteins
/ Male
/ Medicine
/ Myocardial Infarction - blood
/ Myocardial Infarction - genetics
/ Original
/ Tumor Necrosis Factor-alpha - blood
/ Tumor Necrosis Factor-alpha - genetics
/ Tumor Necrosis Factor-alpha - metabolism
/ Ventricular Dysfunction, Left - blood
/ Ventricular Dysfunction, Left - genetics
/ Ventricular Dysfunction, Left - metabolism
