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La expresión de EphA2 regula la inflamación y la remodelación fibroproliferativa en la aterosclerosis

Alexandra C Finney¹, Steven D Funk¹, Jonette M Green¹

¹From Departments of Cell Biology and Anatomy (A.C.F., S.D.F., J.M.G., A. Yurdagul, C.G.K., A.W.O.), Pathology and Translational Pathobiology (J.M.G., A. Yurdagul, R.P., M.H., J.G.T., C.G.K., A.W.O.), Cardiology (M.A.R.), Microbiology and Immunology (A. Yurochko, M.D.W.), and Molecular and Cellular Physiology (C.B.P., C.G.K., A.W.O.), Louisiana State University Health Sciences Center-Shreveport; Departments of Cancer Biology and Cell and Developmental Biology, Vanderbilt University, Nashville, TN (J.C.); and Veterans Affairs Medical Center, Tennessee Valley Healthcare System, Nashville (J.C.).

|May 11, 2017

Resumen

EphA2 (receptor de efrina A2) juega un papel clave en la aterosclerosis, afectando la inflamación de la placa y la progresión. La eliminación de EphA2 reduce la formación de placa aterosclerótica y el desarrollo avanzado de la lesión.

Área de la Ciencia:

Biología cardiovascular
La medicina molecular
Inmunología

Sus antecedentes:

La aterosclerosis implica inflamación crónica y remodelación de las paredes vasculares.
Se observa una expresión elevada de EphA2 en placas ateroscleróticas en humanos y ratones.

Objetivo del estudio:

Investigar el papel de EphA2 en el desarrollo y la progresión de la aterosclerosis.
Para aclarar los mecanismos celulares por los cuales EphA2 influye en la formación de placa aterosclerótica.

Principales métodos:

Se utilizó el nocaut de EphA2 en ratones Apoe-/- alimentados con una dieta occidental.
Evaluó la carga aterosclerótica, los lípidos plasmáticos y realizó experimentos de cultivo celular.
Empleado endotel EphA2 knockdown y quimeras de la médula ósea.

Principales resultados:

Los ratones EphA2-/-Apoe-/- presentaron una reducción de la formación de placa, inflamación y contenido de macrófagos a pesar del aumento de peso y lípidos.
La eliminación endotelial de EphA2 disminuyó la adhesión de los monocitos; la deleción hematopoyética no tuvo ningún efecto.
La deleción de EphA2 redujo la proliferación del músculo liso y la deposición de la matriz extracelular, impidiendo la progresión avanzada de la placa.

Conclusiones:

EphA2 es un nuevo regulador de la inflamación aterosclerótica y la progresión avanzada de la lesión.
El EphA2 endotelial promueve la adhesión de los monocitos, contribuyendo a la inflamación.
El músculo liso EphA2 influye en el desarrollo avanzado de la placa a través de la proliferación y la deposición de la matriz.

Palabras clave:

la aterosclerosis Proliferación de las células Matriz extracelular Fibrosis en el cuerpo inflamación Miocitos, músculo liso

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