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Los fosfolípidos oxidados en las lipoproteínas (a) provocan inflamación de la pared arterial y una respuesta

Fleur M van der Valk¹, Siroon Bekkering¹, Jeffrey Kroon¹

¹From Department of Vascular Medicine (F.M.V.d.V., M.N., E.S.G.S.), Department of Molecular Cell Biology, Sanquin Research (J.K., J.D.v.B.), Experimental Vascular Biology, (J.v.d.B.), Department of Radiology (A.J.N.), and Department of Nuclear Medicine (H.J.V.), Academic Medical Center, Amsterdam, the Netherlands; Departments of Internal Medicine (S.B., L.A.B.J., M.G.N., N.P.R.) and Pharmacology-Toxicology (N.P.R.), Radboud UMC, Nijmegen, the Netherlands; Sulpizio Cardiovascular Center, Division of Cardiovascular Medicine (C.Y., S.T.) and Division of Endocrinology and Metabolism, Department of Medicine (J.L.W.), University California, San Diego, La Jolla; St. Boniface Hospital Research Centre, University of Manitoba, Winnipeg, Canada (A.R.); Department of Chemistry, Biochemistry and Pharmacology, University of Windsor, Windsor, Canada (C.S.); and Robarts Research Institute, Schulich School of Medicine, Western University, London, Canada (M.L.K.).

|August 7, 2016

Resumen

El aumento de la lipoproteína a) [Lp a) ] conduce a la enfermedad cardiovascular al aumentar la inflamación arterial y el tráfico de monocitos. Sus fosfolípidos oxidados (OxPLs) median estos efectos proinflamatorios, ofreciendo un nuevo objetivo terapéutico.

Área de la Ciencia:

Medicina cardiovascular
Inmunología
Biología molecular

Sus antecedentes:

El aumento de la lipoproteína a) [Lp a) ] es un factor de riesgo cardiovascular significativo.
Los mecanismos detrás de la Lp (a) patogenicidad no se comprenden completamente.
Lp (a) contiene fosfolípidos oxidados proinflamatorios (OxPL), lo que sugiere un papel potencial en la atherothrombosis.

Objetivo del estudio:

Investigar los mecanismos por los que la Lp (a) contribuye a la enfermedad cardiovascular.
Determinar el papel de las OxPL en la patogenicidad mediada por Lp.
Para evaluar el efecto de Lp (a) en la función de los monocitos y la inflamación arterial.

Principales métodos:

Imágenes in vivo (IRM, PET/CT, SPECT/CT) para evaluar la carga aterosclerótica y la inflamación.
Análisis ex vivo de los monocitos (FACS, ensayos de migración, ensayos de estimulación).
Estudios in vitro en los que se utilizó un modelo de inmunidad entrenado para investigar las interacciones Lp{\displaystyle Lp}- monocitos.

Principales resultados:

Los sujetos con elevados niveles de Lp (a) mostraron un aumento de la inflamación arterial y el tráfico de monocitos.
Los monocitos de sujetos con niveles elevados de Lp (a) mostraron un estado primado con una mayor migración y producción de citoquinas.
In vitro, Lp (a) aumentó las respuestas proinflamatorias de los monocitos, un efecto dependiente de su contenido de OxPL.

Conclusiones:

Lp (a) promueve el reclutamiento de monocitos en la pared arterial.
El contenido de OxPL de Lp (a) es crucial para mediar respuestas proinflamatorias.
Estos hallazgos aclaran un nuevo mecanismo de enfermedad cardiovascular inducida por Lp.

Palabras clave:

la aterosclerosis Las lipoproteínas Los monocitos

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