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Covalent Binding of BMP-2 on Surfaces Using a Self-assembled Monolayer Approach
Published on: August 26, 2013
La cabeza del antagonista de la BMP regula la fusión de la sutura craneal
Stephen M Warren1, Lisa J Brunet, Richard M Harland
1Department of Surgery, Stanford University School of Medicine, Stanford, California 94305-5148, USA.
Nature
|April 11, 2003
Resumen
Noggin, un antagonista de las proteínas morfogenéticas óseas, es crucial para prevenir la fusión prematura de la sutura craneal. Su supresión por la señalización de FGF2 puede causar craneosinostosis, afectando el desarrollo del cráneo y el crecimiento del cerebro.
Área de la Ciencia:
- Biología del desarrollo Biología del desarrollo.
- Desarrollo craneofacial del cráneo.
- La señalización molecular.
Sus antecedentes:
- Los huesos del cráneo (calvaria) se forman a través de la osificación intramembranosa, con suturas que permiten el crecimiento impulsado por el cerebro.
- La craneosinostosis (fusión de sutura prematura) conduce a una forma anormal del cráneo y problemas de desarrollo.
- Las mutaciones de ganancia de función en los receptores del factor de crecimiento de los fibroblastos (FGFR) están relacionadas con la craneosinostosis síndroma.
Objetivo del estudio:
- Para investigar el papel de Noggin en la permeabilidad de la sutura craneal postnatal.
- Para determinar la relación entre la expresión de Noggin, FGF2 y la señalización de FGFR en el desarrollo de la sutura craneal.
- Para dilucidar el mecanismo por el cual la señalización de FGFR puede contribuir a la craneosinostosis síndroma.
Principales métodos:
- Análisis de la expresión Noggin en suturas craneales postnatales.
- Experimentos in vitro e in vivo que evalúan los efectos de la expresión errónea de Noggin en la fusión de suturas.
- Investigando los efectos supresores de la señalización de FGF2 y FGFR en la expresión Noggin.
Principales resultados:
- Noggin se expresa en suturas de patente, pero está regulado a la baja en suturas de fusión.
- La FGF2 y la señalización FGFR síndroma suprimen la expresión Noggin.
- La mala expresión de Noggin inhibe la fusión de la sutura craneal tanto in vitro como in vivo.
Conclusiones:
- La craneosinostosis síndroma puede surgir de la desregulación inadecuada de Noggin.
- Noggin actúa como un regulador crítico de la permeabilidad de la sutura craneal.
- Dirigirse a la señalización de Noggin podría ofrecer vías terapéuticas para la craneosinostosis.
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