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Cambios de la zona fronteriza NPPB+ conservada desde el programa de genes impulsado por MEF2 al AP1

Karel van Duijvenboden1, Dennis E M de Bakker2, Joyce C K Man1

  • 1Departments of Medical Biology, Amsterdam Cardiovascular Sciences (K.v.D., J.C.K.M., R.J., M.G., I.B.H., P.B., V.M.C.), Academic Medical Center, Amsterdam, The Netherlands.

Circulation
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Las células cardíacas sobrevivientes cerca de un infarto activan un programa de estrés, incluida la expresión de péptido natriurético tipo B (Nppb), crucial para prevenir la insuficiencia cardíaca. Esta respuesta se conserva en los seres humanos.

Palabras clave:
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Área de la Ciencia:

  • Cardiología
  • Biología molecular
  • La genómica

Sus antecedentes:

  • La zona de frontera postinfarto contiene cardiomiocitos sobrevivientes con fluctuaciones microambientales únicas.
  • Estos cardiomiocitos de la zona fronteriza son cada vez más reconocidos por su papel en la regeneración cardíaca.

Objetivo del estudio:

  • Definir las propiedades únicas de transcripción y regulación de los cardiomiocitos de la zona fronteriza.
  • Identificar y validar nuevos marcadores moleculares en la zona fronteriza posterior al infarto.

Principales métodos:

  • Se utilizaron ratones reporteros transgénicos para identificar las zonas fronterizas Nppb positivas después del infarto de miocardio.
  • Se realizó secuenciación de ARN en zonas remotas, fronterizas y de infarto, y núcleos purificados de cardiomiocitos.
  • Se validaron genes candidatos en corazones humanos isquémicos y se evaluó la accesibilidad de la cromatina a través de la secuenciación ATAC.

Principales resultados:

  • Se identificó una zona de frontera transcripcionalmente distinta con un fuerte programa de respuesta al estrés, incluida la regulación a la baja de la fosforilación oxidativa y el metabolismo de los ácidos grasos.
  • Se descubrieron marcadores de zona fronteriza conservados en el corazón humano, incluidos NPPB, ANKRD1, DES, UCHL1, JUN y FOXP1.
  • Demostró que los ratones con deficiencia de Nppb presentan insuficiencia cardíaca letal después del infarto, destacando el papel crítico de Nppb.

Conclusiones:

  • Los cardiomiocitos de la zona fronteriza cambian de un programa impulsado por MEF2 homeostático a un programa inducido por lesiones impulsado por AP-1.
  • Este interruptor de transcripción conservado incluye la expresión de Nppb, esencial para prevenir la insuficiencia cardíaca aguda postinfarto.