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La señalización del FGF regula el crecimiento óseo a través de la autofagia
Laura Cinque1,2, Alison Forrester1,2,3, Rosa Bartolomeo1,2
1Telethon Institute of Genetics and Medicine (TIGEM), Via Campi Flegrei, 34, 80078 Pozzuoli (NA), Italy.
Nature
|November 24, 2015
Resumen
La autofagia, un proceso de reciclaje celular, es crucial para el crecimiento óseo al regular la secreción de colágeno en los condrocitos. La señalización de FGF activa la autofagia, esencial para el desarrollo esquelético y la formación de la matriz extracelular.
Área de la Ciencia:
- Biología celular
- Biología del desarrollo
- Biología esquelética
Sus antecedentes:
- El crecimiento esquelético implica procesos biosintéticos y catabólicos complejos.
- El papel de los procesos catabólicos, como la autofagia, en el crecimiento esquelético no se entiende completamente.
- La autofagia es vital para mantener la homeostasis de los tejidos.
Objetivo del estudio:
- Investigar el papel de la autofagia en los condrocitos durante el crecimiento óseo.
- Para aclarar los mecanismos reguladores de la autofagia en la placa de crecimiento.
- Determinar la relación entre la señalización del FGF y la autofagia en el desarrollo esquelético.
Principales métodos:
- Se ha investigado la inducción de la autofagia en los condrocitos de la placa de crecimiento durante el desarrollo postnatal.
- Se utilizaron ratones que carecían del gen 7 relacionado con la autofagia (Atg7) en los condrocitos.
- Se examinaron los efectos de las deficiencias de Fgf18 y Fgfr4 en la autofagia y los niveles de colágeno.
- Se evaluó el rescate de fenotipos mediante la activación farmacológica de la autofagia.
Principales resultados:
- La autofagia se induce en los condrocitos de la placa de crecimiento postnatalmente y regula la secreción de colágeno tipo II (Col2).
- La deficiencia de Atg7 específica de los condrocitos conduce al almacenamiento en el retículo endoplasmático del procollageno II (PC2) y a la formación defectuosa de la matriz Col2.
- La señalización de FGF18, a través de FGFR4 y JNK, media la inducción de la autofagia postnatal.
- Las deficiencias de Fgf18 y Fgfr4 suprimen la autofagia y disminuyen los niveles de Col2, con fenotipos rescatados por la activación de la autofagia.
Conclusiones:
- La autofagia es un proceso regulado por el desarrollo esencial para el crecimiento óseo.
- La señalización del FGF es un regulador crítico de la autofagia de los condrocitos.
- La autofagia actúa como un nuevo efector de la señalización del FGF en el desarrollo óseo.
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