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H19 Induce el desarrollo y la progresión del aneurisma aórtico abdominal
Daniel Y Li1, Albert Busch1, Hong Jin2
1Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar (D.Y.L., A. Busch, J.P., S.L., H.-H.E., L.M.), Technical University Munich, and German Center for Cardiovascular Research (DZHK), partner site Munich, Germany.
Circulation
|April 20, 2018
Resumen
El ARN largo no codificante H19 regula la supervivencia de las células musculares lisas en el desarrollo del aneurisma aórtico abdominal. La inhibición de H19 puede ofrecer una nueva estrategia terapéutica para la enfermedad del aneurisma aórtico.
Área de la Ciencia:
- Biología molecular
- La genética
- Investigación cardiovascular
Sus antecedentes:
- Los ARN largos no codificantes (ARNlnc) son reguladores clave en los procesos biológicos y las enfermedades.
- El desarrollo del aneurisma aórtico abdominal (AAA) implica mecanismos moleculares complejos.
- La identificación de nuevos lncRNA en la patogénesis de AAA es crucial para el desarrollo terapéutico.
Objetivo del estudio:
- Identificar y caracterizar funcionalmente los lncRNA implicados en el desarrollo del aneurisma aórtico abdominal (AAA).
- Investigar el papel del lncRNA H19 en la patogénesis de la AAA.
- Para explorar el H19 como un objetivo terapéutico potencial para la AAA.
Principales métodos:
- Perfiles de expresión de transcripción de ARN en dos modelos murinos de AAA (infusión de angiotensina II y instilación de elastasa pancreática porcina).
- Reacción en cadena de la transcripción inversa cuantitativa y hibridación in situ para confirmar la expresión de H19.
- Experimentos in vivo e in vitro con oligonucleótidos antisenso (LNA-GapmeRs) para la eliminación de H19 y su sobreexpresión en las células del músculo liso (SMC).
- Análisis de los efectores aguas abajo del H19, incluidos el factor inducible por hipoxia 1α (HIF-1α) y p53.
Principales resultados:
- El lncRNA H19 fue significativamente regulado al alza en ambos modelos AAA murinos.
- La eliminación experimental de H19 redujo el crecimiento del aneurisma y la apoptosis de SMC in vivo.
- La sobreexpresión de H19 aumentó la apoptosis SMC in vitro, independientemente de la miR-675.
- H19 interactúa con HIF-1α en el citoplasma, lo que lleva a la estabilización de p53 y al aumento de la apoptosis SMC.
- H19 promueve la transcripción de HIF-1α mediante el reclutamiento de la proteína de especificidad 1.
Conclusiones:
- El lncRNA H19 es un nuevo regulador de la supervivencia y la apoptosis del SMC en el desarrollo y la progresión del aneurisma aórtico abdominal.
- El H19 juega un papel crítico en la patogénesis de la AAA.
- La inhibición de H19 representa una nueva estrategia terapéutica molecular potencial para la enfermedad del aneurisma aórtico.
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