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La prostaglandina E2 inhibe la elastogénesis en el ducto arterioso a través de la señalización EP4

Utako Yokoyama¹, Susumu Minamisawa, Aki Shioda

¹Cardiovascular Research Institute, Yokohama City University, Yokohama, Japan (U.Y., S.M., A.S., R.I., M.-H.J., Y.I.); the Department of Life Science and Medical Bioscience, Waseda University Graduate School of Advanced Science and Engineering, Tokyo, Japan (S.M., R.I.); the Department of Cell Physiology, Jikei University School of Medicine, Tokyo, Japan (S.M.); the Department of Surgery, Yokohama City University, Yokohama, Japan (M.M.); the Department of Cardiovascular Surgery, Kanagawa Children's Medical Center, Yokohama, Japan (T.A.); the Department of Pharmaceutical Biochemistry, Kumamoto University, Kumamoto, Japan (Y.S.); Cardiovascular Research Institute, Kurume University, Kurume, Japan (H.A.); and the Department of Pharmacology, Kansai Medical University, Osaka, Japan (T.N.).

|October 23, 2013

Resumen

La señalización de la prostaglandina E2 (PGE2) inhibe la formación de fibras elásticas en el ducto arterioso (DA) mediante la degradación de la proteína lisilo oxidasa (LOX), un paso crucial para el establecimiento de la circulación en adultos.

Área de la Ciencia:

Biología Vascular Biología Vascular
Biología del desarrollo Biología del desarrollo.
La bioquímica es la bioquímica.

Sus antecedentes:

La formación de fibra elástica es fundamental para una gran elasticidad arterial durante el desarrollo fetal.
El ducto arterioso (DA) muestra una elastogénesis reducida, lo que facilita su cierre después del nacimiento.
Los mecanismos moleculares de la elastogénesis DA inhibida son en gran parte desconocidos.

Objetivo del estudio:

Para investigar los mecanismos moleculares que regulan la elastogénesis en el ducto arterioso.
Comprender el papel de la señalización de la prostaglandina E2 (PGE2) en el desarrollo de la DA.
Identificar proteínas claves involucradas en la formación diferencial de fibras elásticas entre la AAD y la aorta.

Principales métodos:

Estudió la señalización del receptor de prostaglandina E2 (PGE2) EP4 en el ducto arterioso (DA) y las células del músculo liso aórtico (SMC).
Se utilizó la sobreexpresión mediada por adenovirus de la lisil oxidasa (LOX) en DA SMCs.
Se examinaron ratones con knockout EP4 y se analizaron tejidos humanos de DA y aorta.
Investigó la vía de señalización de la PGE2-EP4-c-Src-fosfolipasa C (PLC) γ.

Principales resultados:

La estimulación del receptor EP4 de la prostaglandina E2 (PGE2) inhibió la elastogénesis y disminuyó la lisilo oxidasa (LOX) en los SMC de DA, pero no en los SMC aórticos.
La sobreexpresión de LOX rescató la inhibición mediada por EP4 de la elastogénesis en DA SMCs.
Los ratones con knockout EP4 exhibieron DA con propiedades elásticas similares a las de la aorta.
Los tejidos humanos mostraron correlaciones inversas entre la formación de fibra elástica, EP4 y la expresión de LOX.
La vía PGE2-EP4-c-Src-PLCγ probablemente promueve la degradación lisosómica de LOX.

Conclusiones:

La señalización de la prostaglandina E2 (PGE2), a través de EP4, inhibe la elastogénesis en el DA promoviendo la degradación de LOX.
La elastogénesis en el DA está regulada espacialmente por la señalización PGE2-EP4.
Este mecanismo es crucial para la transición a la circulación de adultos.

Palabras clave:

la elasticidad la elasticidad.El músculo es liso, suave.pediatría y pediatría.Las prostaglandinas son las prostaglandinas.transducción de señales de transducción de señales.

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