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La insulina induce la regulación al alza de la expresión génica del receptor AT1 vascular por mecanismos
G Nickenig1, J Röling, K Strehlow
1Klinik III für Innere Medizin, Universität Köln, Cologne, Germany.
Circulation
|December 1, 1998
Resumen
La insulina aumenta la expresión del receptor de la angiotensina II AT1 en las células vasculares mediante la estabilización del ARNm, sin afectar la transcripción. Esto puede vincular la hiperinsulinemia con la hipertensión y la aterosclerosis.
Área de la Ciencia:
- Biología Cardiovascular Biología Cardiovascular
- Endocrinología Endocrinología.
- La medicina molecular es una medicina molecular.
Sus antecedentes:
- Las interacciones de insulina y angiotensina II son cruciales en la patogénesis de la aterosclerosis y la hipertensión.
- Comprender estas interacciones es clave para manejar las enfermedades cardiovasculares.
Objetivo del estudio:
- Investigar el efecto de la insulina en la expresión génica del receptor de la angiotensina II AT1 en las células del músculo liso vascular (VSMC).
- Aclarar los mecanismos detrás de la modulación inducida por la insulina de los receptores AT1 y sus consecuencias funcionales.
Principales métodos:
- Los VSMC cultivados fueron tratados con insulina (100 nmol/L) durante 24 horas.
- La densidad del receptor AT1 se midió utilizando ensayos de unión de radioligandos.
- Los niveles de ARNm y la vida media se evaluaron mediante análisis del norte y ensayos nucleares.
- Las respuestas funcionales se evaluaron midiendo la liberación de calcio intracelular.
- La participación de la tirosina quinasa y el calcio intracelular se estudiaron utilizando inhibidores y quelantes específicos.
Principales resultados:
- La insulina aumentó significativamente la densidad de los receptores AT1 (2 veces) y los niveles de ARNm de los receptores AT1 (270+/-20%) en los VSMC.
- La regulación al alza se debió a la prolongación de la vida media del ARNm del receptor AT1 (de 5 a 10 horas), lo que indica una estabilización posttranscripcional.
- La insulina no afectó la transcripción del gen del receptor AT1.
- La insulina pre-incubación aumentó la liberación de calcio intracelular inducida por la angiotensina II, lo que indica un aumento de la función del receptor.
- El efecto de la insulina dependía de las tirosinacinasas y potencialmente involucraba el calcio intracelular.
Conclusiones:
- La insulina regula al alza la expresión del receptor AT1 en los VSMC a través de mecanismos posttranscripcionales, específicamente la estabilización del ARNm.
- Esta regulación del receptor AT1 inducida por la insulina puede explicar el vínculo entre la hiperinsulinemia, la hipertensión y la arteriosclerosis.
- Dirigirse a esta vía podría ofrecer nuevas estrategias terapéuticas para las enfermedades cardiovasculares.
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