Increased FGF8 signaling promotes chondrogenic rather than osteogenic development in the embryonic skull

Disease Models & Mechanisms
Linnea SchmidtTrevor Williams

Abstract

The bones of the cranial vault are formed directly from mesenchymal cells through intramembranous ossification rather than via a cartilage intermediate. Formation and growth of the skull bones involves the interaction of multiple cell-cell signaling pathways, with fibroblast growth factors (FGFs) and their receptors exerting a prominent influence. Mutations within the FGF signaling pathway are the most frequent cause of craniosynostosis, which is a common human craniofacial developmental abnormality characterized by the premature fusion of the cranial sutures. Here, we have developed new mouse models to investigate how different levels of increased FGF signaling can affect the formation of the calvarial bones and associated sutures. Whereas moderate Fgf8 overexpression resulted in delayed ossification followed by craniosynostosis of the coronal suture, higher Fgf8 levels promoted a loss of ossification and favored cartilage over bone formation across the skull. By contrast, endochondral bones were still able to form and ossify in the presence of increased levels of Fgf8, although the growth and mineralization of these bones were affected to varying extents. Expression analysis demonstrated that abnormal skull chondrogenesis was...Continue Reading

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Citations

Jul 2, 2019·Chemical Biology & Drug Design·Jicheng WangZhi Yi
Apr 4, 2019·The Chinese Journal of Physiology·Tsung-Ming ChenShaw-Jenq Tsai
Oct 5, 2019·Advanced Healthcare Materials·Jinglun ZhangYufeng Zhang
Aug 19, 2020·Nature Reviews. Rheumatology·Yangli XieMoosa Mohammadi
Sep 4, 2020·Signal Transduction and Targeted Therapy·Yangli XieLin Chen
Jan 15, 2021·Stem Cell Research·Takayoshi OtsukaCato T Laurencin

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Datasets Mentioned

BETA
GSE112413

Methods Mentioned

BETA
PCR
RNAseq
glycosylation
transgenic
genotyping

Software Mentioned

DAVID
Cufflinks
gSNAP
R

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