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Beta-Arrestin1 Previene la preeclampsia mediante la regulación a la baja de los heterómeros del receptor AT1-B2

Ursula Quitterer¹, Xuebin Fu², Armin Pohl³

¹Molecular Pharmacology, Department of Chemistry and Applied Biosciences, ETH Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland; Department of Medicine, Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.

|December 4, 2018

Resumen

Los síntomas de la preeclampsia en ratones fueron prevenidos mediante la orientación de los complejos receptores. Este hallazgo ofrece un nuevo enfoque terapéutico prometedor para esta complicación común del embarazo.

Área de la Ciencia:

Obstetricia y ginecología
Investigación cardiovascular
La medicina molecular

Sus antecedentes:

La preeclampsia es una de las principales causas de complicaciones del embarazo en todo el mundo, y carece de tratamientos efectivos.
Los impulsores moleculares precisos de la preeclampsia siguen siendo incompletamente entendidos.
Los receptores acoplados a proteínas G juegan un papel crítico en la función vascular.

Objetivo del estudio:

Investigar el papel de las interacciones de los receptores de la angiotensina II AT1 y bradicinina B2 en la patogénesis de la preeclampsia.
Identificar posibles objetivos terapéuticos para la preeclampsia basados en la heteromerización de los receptores.

Principales métodos:

Utilizó un modelo de ratón de la preeclampsia.
Examinó la formación compleja entre los receptores AT1 y B2.
Se evaluó la señalización del calcio y la mecanicidad del músculo liso vascular.
Investigó el papel de la beta-arrestina en la desregulación de los receptores.
Intervenciones terapéuticas evaluadas, incluida la expresión transgénica de ARRB1 y un fármaco de molécula pequeña.
Analizó las biopsias de la placenta humana.

Principales resultados:

Se observó un aumento de la formación del complejo de receptores AT1-B2 en ratones preñados, correlacionado con los síntomas de preeclampsia.
La heteromerización aberrante de AT1-B2 condujo a una exagerada señalización de calcio y a un aumento de la mecanosensibilidad vascular.
La desregulación mediada por betaarrestina inhibió la agregación de los receptores AT1-B2.
La expresión transgénica de ARRB1 y un fármaco de molécula pequeña previnieron los síntomas de preeclampsia en ratones.
Se detectó heteromerización AT1-B2 en los tejidos placentarios preeclampticos humanos.

Conclusiones:

La heteromerización aberrante del receptor AT1-B2 es un mecanismo clave que desencadena los síntomas de la preeclampsia.
Dirigirse a la heteromerización AT1-B2 y sus efectos posteriores presenta una nueva estrategia terapéutica para la preeclampsia.
Esta investigación ofrece una vía potencial para desarrollar tratamientos efectivos para la preeclampsia.

Palabras clave:

AGTR1 y sus derivados Se incluyen los siguientes elementos:BDKRB2 y BDKRB2 Amlodipino y sus derivados La angiotensina II también está presente.agonista sesgado Bradiquinina y sus derivados El heterodímero Mecanosensibilidad Preeclampsia, por ejemplo

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