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La proliferación de células del músculo liso inducida por las lipoproteínas residuales implica la transactivación del
Akio Kawakami1, Akira Tanaka, Tsuyoshi Chiba
1Department of Medical Biochemistry, Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Building D-256, Bunkyo-ku, Tokyo 113-8519, Japan.
Circulation
|November 19, 2003
Resumen
Las lipoproteínas residuales (RLPs) promueven la proliferación de las células del músculo liso (SMC) mediante la activación de la vía del receptor del factor de crecimiento epidérmico (EGF). Este mecanismo involucra la proteína quinasa C (PKC) y el factor de crecimiento similar al EGF que se une a la heparina (HB-EGF), lo que contribuye al desarrollo de la aterosclerosis.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- La señalización celular.
- Investigación de la aterosclerosis Investigación de la aterosclerosis.
Sus antecedentes:
- Las lipoproteínas residuales (RLP) están implicadas en la aterosclerosis.
- La proliferación de células del músculo liso vascular (SMC) es clave en la aterosclerosis y la restenosis.
- El impacto directo de los RLP en las SMC requiere una mayor aclaración.
Objetivo del estudio:
- Investigar los efectos directos de los RLP en la proliferación de las SMC.
- Para explorar las vías de transducción de señales involucradas en las respuestas SMC mediadas por RLP.
Principales métodos:
- Las SMC aórticas de la rata fueron incubadas con RLP.
- Se midió la proliferación celular.
- Se evaluó la fosforilación de las proteínas (receptor EGF, MAPK) y el derramamiento (HB-EGF).
- Se utilizaron inhibidores de la PKC, metaloproteasas y anticuerpos neutralizantes del HB-EGF.
- Los experimentos se llevaron a cabo en ratones apolipoproteína E-knockout y C57BL6.
Principales resultados:
- Las RLPs aumentaron significativamente la proliferación de SMC (2,3 veces).
- Las RLPs indujeron la fosforilación del receptor EGF, la posterior activación de MAPK y la activación de PKC.
- El tratamiento con RLP condujo a la secreción de HB-EGF, que fue inhibida por PKC e inhibidores de la metaloproteasa.
- La transactivación del receptor EGF y el derramamiento de HB-EGF fueron bloqueados por un anticuerpo anti-HB-EGF.
- Estos eventos moleculares se observaron in vivo en modelos de ratón de aterosclerosis.
Conclusiones:
- Las RLPs estimulan la proliferación de SMC a través de la transactivación del receptor del FEAG.
- Esta transactivación está mediada por la activación de PKC y el derramamiento de HB-EGF.
- Estos hallazgos ponen de relieve un nuevo mecanismo que vincula las RLP con la proliferación vascular de células del músculo liso en la aterosclerosis.
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