Key result
Specific ribosomal proteins show distinct upregulation in CABG and hyperlipidemia models but decrease following MI.
Why the study?
The extra ribosomal functions of ribosomal proteins released under ischemic insults in cardiac tissue and epicardial fat are unknown.
Swine model data should not yet inform clinical decisions; leaves open ribosomal protein roles in human LV remodeling.
Sustenance of ischemia in the surviving cardiac tissue following myocardial infarction (MI) elicits a proinflammatory milieu resulting in subsequent pathological episodes. Also, the activation and release of ribosomal proteins under ischemic insults have been unveiled; however, their extra ribosomal functions are unknown. We identified the ribosomal proteins including RPL10A, RPL14, RPL30, RPS18, FAU-40 (RPS30), and RPSA (Laminin Receptor, LR) in the vesicles of ischemia challenged epicardial adipose tissue derived stromal cells (EATDS). The present study aimed to assess the association of these proteins in the epicardial adipose tissues (EAT) and left ventricular (LV) myocardium and isolated stromal cells (EATDS and LVSCs) from hyperlipidemic (HL), MI and coronary artery bypass graft (CABG) swine models. The findings revealed an upregulation of RPL10A, RPL14, RPL30, RPS18, RPS30, and RPSA in the LV tissues of CABG and HL swine with a concomitant reduction in the MI group. RPS30 displayed similar upregulation in EAT, whereas the expression of other ribosomal proteins was not significantly altered. Additionally, the ischemic LVSCs and EATDS displayed altered expression status of these genes compared to the control. Also, the RPS18 + , RPL30 + and RPSA + LVSCs favored ischemia and revealed similar anti-inflammatory and regenerative sub-phenotypes reflecting the protective/survival mechanisms. Further understanding regarding the underlying molecular mechanisms and functions of these ribosomal proteins offers immense translational opportunities in the better management of ischemic cardiac complications.
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Thai et al. (2024) studied Myocardial infarction, hyperlipidemia, and CABG (swine models). Hyperlipidemia, MI, and CABG models vs. Control was evaluated on Expression of ribosomal proteins in LV tissues and epicardial adipose tissues. Ribosomal proteins RPL10A, RPL14, RPL30, RPS18, RPS30, and RPSA were upregulated in the LV tissues of CABG and hyperlipidemic swine models, with a concomitant reduction in the MI group.
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