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Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
Published on: October 12, 2017
Protección contra la muerte de las células endoteliales vasculares inducida por lipoproteínas de baja densidad
1Department of Radiation Oncology, Duke University Medical Center, Durham, NC, USA.
Circulation
|December 6, 2001
Resumen
La quinasa ligada a la integrina (ILK) protege las células endoteliales vasculares de la apoptosis inducida por el LDL oxidado (oxLDL). La upregulación de la ILK puede prevenir la lesión de las células endoteliales en la aterosclerosis.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- La señalización celular de las células.
- La medicina molecular es una medicina molecular.
Sus antecedentes:
- La quinasa ligada a la integrina (ILK) es crucial para la señalización de la matriz extracelular y se expresa preferentemente en los tejidos musculares.
- ILK actúa como un regulador aguas arriba de la proteína quinasa B, un mediador clave de la apoptosis.
- El LDL oxidado (oxLDL) está implicado en la aterogénesis a través de la apoptosis de las células endoteliales.
Objetivo del estudio:
- Investigar el papel de la ILK en la apoptosis inducida por el LDL oxidado (oxLDL) en las células endoteliales vasculares.
- Para determinar si ILK influye en las vías de señalización involucradas en la muerte celular inducida por oxLDL.
Principales métodos:
- Investigó la transcripción y la traducción del gen ILK utilizando la reacción en cadena de la polimerasa de transcripción inversa y el análisis occidental.
- Utilizó un vector de adenovirus recombinante para la sobreexpresión del gen ILK en las células endoteliales.
- Se evaluó la apoptosis utilizando dos métodos de ensayo independientes y se analizaron los factores clave relacionados con la apoptosis (bcl-2, bcl-xl, caspase 3, caspase 9) y la actividad de p38 MAPK.
Principales resultados:
- El tratamiento de LDL oxidado (oxLDL) aumentó tanto la transcripción como la traducción del gen ILK en las células endoteliales.
- La sobreexpresión de ILK inhibió significativamente la apoptosis inducida por oxLDL y la muerte celular tanto en la vena umbilical humana como en las células endoteliales de la vena linfoide de ratón transformadas por el virus simio 40.
- ILK suprimió la activación inducida por oxLDL de la proteína quinasa activada por mitógeno p38 y moduló la expresión de proteínas relacionadas con la apoptosis.
Conclusiones:
- La quinasa ligada a la integrina (ILK) juega un papel regulador significativo en la prevención de la apoptosis inducida por el LDL oxidado (oxLDL) en las células endoteliales vasculares.
- La modulación de la actividad de ILK presenta una estrategia terapéutica potencial para prevenir el daño de las células endoteliales en la aterosclerosis.
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