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Existe un sistema de inducción/activación de la metaloproteinasa matriz en el miocardio ventricular izquierdo humano

F G Spinale¹, M L Coker, L J Heung

¹Medical University of South Carolina, Charleston 29425, USA.

|October 18, 2000

Resumen

Las metaloproteinasas matriciales (MMP) y sus inductores (EMMPRIN, MT1-MMP) están regulados al alza en la cardiomiopatía dilatada (DCM) con insuficiencia cardíaca. Dirigirse a estos MMP en el ventrículo izquierdo ofrece una potencial estrategia terapéutica para la DCM.

Área de la Ciencia:

Biología Cardiovascular Biología Cardiovascular
La medicina molecular es una medicina molecular.
La bioquímica es la bioquímica.

Sus antecedentes:

Las metaloproteinasas de matriz (MMP) son clave en la remodelación de la matriz durante la enfermedad, incluida la metástasis tumoral.
El inductor de la metaloproteinasa de matriz extracelular (EMMPRIN) y el MMP de tipo membrana (MT1-MMP) están implicados en la regulación del MMP.
La expresión y la actividad de EMMPRIN y MT1-MMP en el miocardio ventricular izquierdo (LV) humano en cardiomiopatía dilatada (DCM) siguen siendo en gran medida no caracterizadas.

Objetivo del estudio:

Para investigar la expresión de EMMPRIN y MT1-MMP en el miocardio LV humano.
Evaluar la asociación de EMMPRIN y MT1-MMP con la actividad y expresión de MMP en DCM.
Para explorar posibles blancos terapéuticos en el corazón humano que falla.

Principales métodos:

Análisis del tejido miocárdico LV de pacientes con DCM no isquémica e isquémica, y controles normales.
Zimografía para evaluar la actividad de MMP.
Análisis cuantitativo de los niveles de expresión de MMP, EMMPRIN y MT1-MMP.

Principales resultados:

La actividad de MMP en el miocardio de LV fue significativamente elevada (> 2 veces) tanto en la DCM no isquémica como en la isquémica en comparación con los controles normales.
La abundancia de MMP-9, MMP-2 y MMP-3 aumentó en el DCM, mientras que los niveles de MMP-1 disminuyeron.
La expresión de EMMPRIN aumentó en >250% y MT1-MMP en >1000% en ambos grupos de DCM.

Conclusiones:

La miocardiopatía dilatada se caracteriza por un aumento de la actividad MMP miocárdica de LV y una regulación al alza selectiva de MMP.
Un sistema local de inducción / activación de MMP que involucra EMMPRIN y MT1-MMP está presente y regulado hacia arriba en los miocitos LV humanos que fallan.
La modulación de la activación y la expresión de MMP en el miocardio LV humano que falla presenta una nueva vía terapéutica para DCM.

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