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Small ubiquitin-related modifier 1 (SUMO1) is a protein family member involved in post-translational modification resulting in cellular processes such as transcriptional regulation, cell signaling, apoptosis and protein stability. It has been shown that SUMO1 indirectly represses oxidative stress ameliorating cellular damage. Therapeutic use has been proposed in heart failure, however we aimed to identify differential SUMO1 gene expression between stable angina (SA) patients and controls along with a correlation with plaque morphology, providing a potential therapeutic target for atherosclerotic plaque modulation.
We recruited 48 patients with SA undergoing frequency domain optical coherence tomography-guided (FD-OCT) percutaneous coronary intervention (PCI) and 33 age/sex matched controls. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed using a custom micro-array from isolated ribonucleic acid. Subjects with diabetes, renal impairment, left ventricular impairment, bleeding diathesis, contraindication to antiplatelets, malignancy, active inflammatory disease and prior coronary revascularization were excluded.
SUMO1 expression was significantly down regulated in SA versus control (p<0.001). A positive correlation existed between qRT-PCR cycle threshold (Ct) and lipid arc (Spearman’s Correlation: rs=0.45, p=0.001). Higher Ct corresponds with lower mRNA transcripts, hence lower SUMO1 gene expression correlated with a higher lipid arc.
SUMO1 was significantly down-regulated in SA versus controls and lower expression correlated with higher lipid arc, presenting a potential lipid modifying target in atherosclerotic plaque.