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Se requiere la inducción de microARN-199 por el óxido nítrico en las células endoteliales para la resistencia a los

Yong-Ping Bai1,2, Jia-Xiong Zhang1, Quan Sun3

  • 1Department of Geriatric Medicine (Y.-P.B., J.-X.Z., L.-F.H., W.-Z.W.).

Circulation
|February 13, 2018
PubMed
Resumen
Este resumen es generado por máquina.

La tolerancia al nitrato, una complicación del tratamiento de la enfermedad arterial coronaria, es causada por el microARN-199 (miR-199) que reprime la prostaglandina I2 sintasa (PTGIS). La inhibición de miR-199 puede restaurar la eficacia del nitrato.

Palabras clave:
MIRN199 microARN en ratasEnfermedad arterial coronariacélulas endotelialesLos nitratosÓxido nítriconitroglicerina y sus derivadosLas prostaglandinas I

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Área de la Ciencia:

  • Biología cardiovascular
  • La medicina molecular
  • La epigenética

Sus antecedentes:

  • Los nitratos son cruciales para el tratamiento de la enfermedad arterial coronaria, pero la eficacia está limitada por la tolerancia a los nitratos.
  • La tolerancia al nitrato está relacionada con la disfunción de la prostaglandina I2 sintasa (PTGIS).
  • Los microARN (miRNA) son reguladores epigenéticos clave de la función endotelial, que influyen en la expresión génica.

Objetivo del estudio:

  • Investigar si los nitratos inducen la resistencia a los nitrovasodilatadores a través de la represión del gen PTGIS dependiente del miARN.
  • Aclarar el papel del microARN-199 (miR-199) en el desarrollo de la tolerancia a los nitratos.

Principales métodos:

  • Inducción de la resistencia a los nitrovasodilatadores en ratones Apoe-/- mediante infusión de nitroglicerina.
  • Evaluación de las respuestas de la arteria aórtica a los donantes de óxido nítrico en una cámara de órganos.
  • Cuantificación de la expresión de miR-199a/b mediante la qRT-PCR y el FISH.

Principales resultados:

  • Los donantes de óxido nítrico aumentaron miR-199a/b y disminuyeron la expresión de PTGIS en las células endoteliales.
  • miR-199a/b se dirige directamente al ARNm PTGIS, lo que lleva a su degradación.
  • En ratones, la nitroglicerina indujo la miR-199a/b, disminuyó el PTGIS y causó resistencia a los nitrovasodilatadores, que fue revertida por la inhibición de la miR-199a/b.
  • En los seres humanos, los niveles elevados de miR-199a/b se correlacionaron con la tolerancia al nitrato.

Conclusiones:

  • El aumento de la regulación endotelial de miR-199a/b es esencial para la resistencia a los nitrovasodilatadores mediante la represión del PTGIS.
  • miR-199a/b representa un nuevo objetivo terapéutico para superar la tolerancia a los nitratos en las enfermedades cardiovasculares.