Increased Expression of Inactive Rhomboid Protein 2 in Circulating Monocytes after Acute Myocardial Infarction.
Abstract
Increased TNF-alpha levels following acute myocardial infarction (AMI) contribute to impaired recovery of myocardial function. Interaction of inactive rhomboid protein 2 (iRhom2) with TNF-alpha converting enzyme (TACE) is required for TNF-alpha shedding from immune cells. We hypothesized that iRhom2 expression increases in circulating monocytes following AMI. Transcript levels of iRhom2, TACE and TNF-alpha 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-alpha and TACE mRNA expression remained unchanged. At d3, iRhom2 mRNA expression positively correlated with levels of intermediate monocytes or serum TNF-alpha, 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.
Authors: | van Dijck P, Hannemann C, Dreger H, Stangl V, Stangl K, Ludwig A, Hewing B, |
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Journal: | J Cardiovasc Transl Res;2024May14. doi:10.1007/s12265-024-10519-5 |
Year: | 2024 |
PubMed: | PMID: 38743187 (Go to PubMed) |