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Las células endoteliales regulan el crecimiento fisiológico de los cardiomiocitos a través de la señalización
Riikka Kivelä1, Karthik Amudhala Hemanthakumar1, Katri Vaparanta2,3
1Wihuri Research Institute, Helsinki, Finland and Translational Cancer Biology Program, Research Programs Unit, Faculty of Medicine, University of Helsinki, Finland (R.K., K.A.H., M.R., K.A.).
Circulation
|March 30, 2019
Resumen
Las células endoteliales y los cardiomiocitos se comunican a través de vías de señalización para coordinar el crecimiento fisiológico cardíaco y la hipertrofia. Esta conversación cruzada es crucial para mantener la función cardíaca durante el aumento de la vascularización.
Área de la Ciencia:
- Biología cardiovascular
- Señalización celular
- Investigación de la angiogénesis
Sus antecedentes:
- La insuficiencia cardíaca es un problema de salud mundial importante a menudo precedido por hipertrofia cardíaca patológica.
- La expansión vascular cardíaca es crítica para determinar el crecimiento fisiológico frente al patológico del corazón.
- El diálogo cruzado entre células endotelial (CE) y cardiomiocito (CMC) regula el crecimiento cardíaco, pero los mecanismos siguen sin estar claros.
Objetivo del estudio:
- Esclarecer los mecanismos de interacción EC-CMC en el crecimiento cardíaco.
- Identificar las señales derivadas de la CE que regulan la homeostasis de la CMC.
- Comprender cómo la angiogénesis influye en la hipertrofia cardíaca e identificar objetivos terapéuticos para la insuficiencia cardíaca.
Principales métodos:
- Se utilizaron modelos genéticos de ratón para eliminar los receptores VEGF.
- Se emplean vectores virales asociados a la adeno para la transducción miocárdica.
- Se han realizado experimentos de cultivo celular y análisis moleculares (qPCR, microarrays, ELISA, IHC).
Principales resultados:
- La deleción EC de VEGFR1 y la entrega del ligando VEGFR1 aumentaron la vasculatura coronaria y indujeron hipertrofia fisiológica de CMC.
- La señalización del VEGF a través del VEGFR2 endotelial medió estos efectos, bloqueados por la inhibición del VEGFR2.
- Se identificaron las vías de Notch y ErbB como mediadores clave del diálogo cruzado EC-CMC.
Conclusiones:
- Las vías de señalización EC VEGFR2 y CMC ErbB coordinan la hipertrofia CMC con la angiogénesis.
- Esta conversación cruzada contribuye al crecimiento cardíaco fisiológico.
- Los hallazgos ofrecen información sobre nuevas estrategias terapéuticas para la insuficiencia cardíaca.
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