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Inhibiting Receptor Prevents Craniosynostosis in Mice

Uncoupling Fgfr2 from downstream signaling components reverses fusion of skull sutures in mouse Crouzon syndrome model

WEDNESDAY, Nov. 29 (HealthDay News) -- Blocking the fibroblast growth factor receptor 2 (Fgfr2) pathway could help in treatment of craniosynostosis and other bone disorders, according to a report published online Nov. 28 in the Proceedings of the National Academy of Sciences Early Edition.

Joseph Schlessinger, Ph.D., of Yale University School of Medicine in New Haven, Conn., and colleagues used a mouse model of Crouzon syndrome, which carry an overactive version of Fgfr2c and develop craniosynostosis, to determine the downstream signaling components required for the disease.

The investigators found that mice carrying the overactive Fgfr2c allele plus an additional mutation that uncouples Fgfr2c from the docking protein Frs2α regained normal skull development. Pharmacological inhibition of Fgfr2 signaling also corrected Crouzon-like fusions in an organ culture model.

The authors conclude that "modalities that attenuate signaling pathways stimulated by pathologically activated FGFRs could be applied for treatment of craniosynostosis and other severe bone deformities caused by activated FGFR mutants, which currently do not have any treatments."

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