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La pérdida de Wnt5a derivado del endotelio está asociada con la reducción del reclutamiento de pericitos y la pérdida

Ke Yuan1,2,3, Elya A Shamskhou1,2,3, Mark E Orcholski1,2,3

  • 1Division of Pulmonary and Critical Care Medicine (K.Y., E.A.S., M.E.O., A.N., V.A.d.J.P.), Stanford University, Palo Alto, CA.

Circulation
|December 28, 2018
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Resumen

La hipertensión arterial pulmonar (HAP) implica un deterioro en el reclutamiento de pericitos debido a una baja señalización de Wnt5a. La restauración de Wnt5a puede prevenir la pérdida de microvasculares en la HAP.

Palabras clave:
En el caso de los vehículos de motor:células endotelialesLos exosomasLos pericitoshipertensión pulmonar

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Área de la Ciencia:

  • Investigación cardiovascular
  • Biología celular
  • Medicina de los pulmones

Sus antecedentes:

  • La hipertensión arterial pulmonar (HAP) se caracteriza por la pérdida de microvasculares y la regeneración deteriorada.
  • La reducción de la cobertura pericital de los micro vasos pulmonares es una característica patológica clave en la HAP.
  • La disfunción pericital en la HAP se debe en parte a una respuesta alterada a las señales de las células endotelial microvasculares pulmonares (CEMP).

Objetivo del estudio:

  • Investigar el papel de los ligandos Wnt producidos por las PMVEC en la activación de la vía de polaridad Wnt/célula plana en los pericitos.
  • Determinar si el Wnt5a producido por las PMVEC es esencial para el reclutamiento de pericitos y la integridad de los microvasculares pulmonares.

Principales métodos:

  • Aislamiento de pericitos y PMVEC de pulmones sanos y de HAP.
  • PCR cuantitativa para analizar la expresión de Wnt en los PMVEC.
  • Purificación y caracterización del exosoma.
  • Evaluación de la hipertensión pulmonar y la función del ventrículo derecho en un modelo de ratón noqueado específico del endotelio Wnt5a.

Principales resultados:

  • Los PMVEC sanos cocultivados con pericitos mostraron un aumento de 35 veces en la expresión de Wnt5a, a diferencia de los PMVEC con HAP.
  • Los niveles de Wnt5a en los exosomas de los PMVEC sanos aumentaron con el cocultivo de pericitos, pero no en los HAP.
  • La adición de Wnt5a o exosomas PMVEC saludables promovió el reclutamiento de pericitos en los PMVEC de HAP.
  • Los ratones con Wnt5a knockout presentaron hipertensión pulmonar persistente e insuficiencia ventricular derecha después de la recuperación de la hipoxia, con una reducción de la cobertura de pericitos microvasculares.

Conclusiones:

  • Wnt5a se ha identificado como un mediador crucial de las interacciones entre el endotelio pulmonar y los pericitos.
  • La pérdida de Wnt5a puede contribuir a la HAP al comprometer la viabilidad de los microvasculares pulmonares recién formados.
  • Las terapias dirigidas a restaurar la producción de Wnt5a podrían prevenir la pérdida de microvasculares en la HAP.