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'Atherothrombosis-associated microRNAs in Antiphospholipid syndrome and Systemic Lupus Erythematosus patients'
C Pérez-Sánchez1, M A Aguirre1, P Ruiz-Limón1
1Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC)/Reina Sofia University Hospital/University of Cordoba, Cordoba, Spain.
Abstract:
MicroRNAs markedly affect the immune system, and have a relevant role in CVD and autoimmune diseases. Yet, no study has analyzed their involvement in atherothrombosis related to APS and SLE patients. This study intended to: 1) identify and characterize microRNAs linked to CVD in APS and SLE; 2) assess the effects of specific autoantibodies. Six microRNAs, involved in atherothrombosis development, were quantified in purified leukocytes from 23 APS and 64 SLE patients, and 56 healthy donors. Levels of microRNAs in neutrophils were lower in APS and SLE than in healthy donors. Gene and protein expression of miRNA biogenesis-related molecules were also reduced. Accordingly, more than 75% of identified miRNAs by miRNA profiling were underexpressed. In monocytes, miR124a and -125a were low, while miR-146a and miR-155 appeared elevated. Altered microRNAs' expression was linked to autoimmunity, thrombosis, early atherosclerosis, and oxidative stress in both pathologies. In vitro treatment of neutrophils, monocytes, and ECs with aPL-IgG or anti-dsDNA-IgG antibodies deregulated microRNAs expression, and decreased miRNA biogenesis-related proteins. Monocyte transfections with pre-miR-124a and/or -125a caused reduction in atherothrombosis-related target molecules. In conclusion, microRNA biogenesis, significantly altered in neutrophils of APS and SLE patients, is associated to their atherothrombotic status, further modulated by specific autoantibodies.
Insights
MicroRNA biogenesis is altered in neutrophils of Antiphospholipid Syndrome (APS) and Systemic Lupus Erythematosus (SLE) patients, impacting their risk of atherothrombosis. Autoantibodies further modify these microRNA changes.
Area of Science:
- Immunology
- Molecular Biology
- Cardiovascular Science
Background:
- MicroRNAs play a crucial role in immune regulation and are implicated in cardiovascular disease (CVD) and autoimmune conditions.
- Atherothrombosis is a significant complication in patients with Antiphospholipid Syndrome (APS) and Systemic Lupus Erythematosus (SLE).
- The specific involvement of microRNAs in atherothrombosis within APS and SLE patient cohorts remains largely unexplored.
Purpose of the Study:
- To identify and characterize microRNAs associated with CVD in APS and SLE patients.
- To investigate the impact of specific autoantibodies on microRNA expression and function.
- To elucidate the role of microRNA dysregulation in the atherothrombotic processes observed in APS and SLE.
Main Methods:
- Quantification of six key microRNAs in purified leukocytes from APS patients, SLE patients, and healthy donors.
- Analysis of gene and protein expression of microRNA biogenesis-related molecules.
- In vitro experiments involving autoantibody treatment of immune cells and endothelial cells (ECs), and microRNA transfections in monocytes.
Main Results:
- Neutrophil microRNA levels were significantly reduced in both APS and SLE patients compared to healthy controls.
- MicroRNA biogenesis-related molecules were downregulated, with over 75% of identified microRNAs underexpressed.
- Specific microRNAs (miR-124a, -125a, -146a, -155) showed altered expression in monocytes, linked to autoimmunity, thrombosis, and oxidative stress.
- Autoantibodies (aPL-IgG, anti-dsDNA-IgG) deregulated microRNA expression and reduced biogenesis-related proteins in vitro.
- Monocyte transfection with specific microRNAs reduced atherothrombosis-related target molecules.
Conclusions:
- MicroRNA biogenesis is significantly altered in neutrophils of APS and SLE patients, correlating with their atherothrombotic state.
- Specific autoantibodies modulate microRNA expression and contribute to the observed alterations.
- Targeted manipulation of microRNAs holds potential for therapeutic strategies against atherothrombosis in these autoimmune diseases.
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