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El LDL enzimáticamente degradado y no oxidado induce la activación de las células musculares lisas vasculares

M Klouche¹, S Rose-John, W Schmiedt

¹Institute of Medical Microbiology, University of Mainz, Germany. klouche@mail.uni-mainz.de

|April 19, 2000

Resumen

La LDL modificada enzimáticamente (E-LDL) desencadena la proliferación de las células del músculo liso vascular (SMC) y altera su expresión génica, contribuyendo al desarrollo temprano de la lesión aterosclerótica.

Área de la Ciencia:

Biología Cardiovascular Biología Cardiovascular
Investigación de la aterosclerosis Investigación de la aterosclerosis.
La Medicina Celular y Molecular.

Sus antecedentes:

La modificación enzimática y no oxidativa del LDL crea una forma aterogénica (E-LDL).
La E-LDL activa el complemento y los macrófagos, apareciendo en las primeras lesiones ateroscleróticas.

Objetivo del estudio:

Para investigar los efectos aterogénicos de E-LDL en las células del músculo liso vascular humano (SMC).

Principales métodos:

Evaluación de la acumulación de E-LDL en SMC.
Expresión génica medida de las quimiocinas y proteínas inflamatorias.
Se analizó la señalización de la familia gp130 y del receptor IL-6 (IL-6R).
Se han investigado los mecanismos de proliferación de SMC inducidos por E-LDL.

Principales resultados:

E-LDL acumulado en SMC, induciendo selectivamente la proteína quimiotáctica monocítica-1.
El E-LDL estimula la expresión de gp130 y la secreción de IL-6.
El E-LDL promovió la proliferación de SMC a través de los circuitos del factor de crecimiento autocrino y la transseñalización de IL-6/sIL-6R.
La IL-6 derivada de los macrófagos y el receptor de IL-6 soluble (sIL-6R) aumentaron la proliferación de SMC.

Conclusiones:

E-LDL induce alteraciones en el SMC característico de la evolución de las lesiones ateroscleróticas.
E-LDL contribuye a los cambios celulares observados en la aterosclerosis temprana.

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