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Increased FGF8 Signaling Promotes Chondrogenic Rather Than Osteogenic Development in the Embryonic Skull

ABSTRACT: Increased FGF8 Signaling Promotes Chondrogenic Rather Than Osteogenic Development in the Embryonic Skull

PROVIDER: PRJNA445954 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6907110.fastq.gz	Fastqsanger.gz
	SRR6907111.fastq.gz	Fastqsanger.gz
	SRR6907112.fastq.gz	Fastqsanger.gz
	SRR6907104.fastq.gz	Fastqsanger.gz
	SRR6907105.fastq.gz	Fastqsanger.gz

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

Project description: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 accompanied by changes in the genes required for Wnt signaling. Moreover, further analysis indicated that the pathology was associated with decreased Wnt signaling, as the reduction in ossification could be partially rescued by halving Axin2 gene dosage. Taken together, these findings indicate that mesenchymal cells of the skull are not fated to form bone, but can be forced into a chondrogenic fate through the manipulation of FGF8 signaling. These results have implications for evolution of the different methods of ossification as well as for therapeutic intervention in craniosynostosis.

| S-EPMC6031357 | biostudies-literature

Increased FGF8 Signaling Promotes Chondrogenic Rather Than Osteogenic Development in the Embryonic Skull

Project description:RNA-seq of RNA isolated from E14.5 mouse embryos- wildtype cranial base tissue, Msx2-Cre;CAGFgf8 mutant cranial vault, and wildtype cranial vault; 3 replicates of each group.

2018-05-23 | GSE112413 | GEO

Fgf8 signaling alters the osteogenic cell fate in anterior hard palate

Project description:FGF signaling has been implicated in the regulation of osteogenesis in both intramembranous and endochondral ossification. In the developing palate, the anterior bony palate forms by direct differentiation of cranial neural crest-derived mesenchymal cells, but the signals that regulate osteogenic cell fate remains unclear. In the present study, we present evidence that locally activated FGF8 signaling in the anterior palate leads to complete bone loss of the palatine process of the maxilla (ma) and ectopic cartilage formation. This aberrant developmental process was accompanied by significantly elevated level of cell proliferation, which contributes to abnormally thickened ma, and complete inhibition of Osterix expression, which accounts for the lack of bone formation. Consistent with the phenotype, RNA-Sequencing (RNA-Seq) analysis further demonstrated that augmented FGF8 signaling downregulated genes involved in ossification, biomineral tissue development, and bone mineralization, but upregulated genes involved in cell proliferation, cartilage development, and cell fate commitment. Expression validation of selected genes supported the RNA-Seq results. We conclude that FGF signaling functions as a negative regulator of osteogenic fate but promotes chondrogenesis of cranial neural crest cell-derived mesenchyme in the hard palate, which will have implication in directed differentiation of precursor cells for clinical application.

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Identification of differentially-expressed miRNAs in early osteogenic and chondrogenic differentiation of human bone marrow-mesenchymal stromal cells (hMSCs)

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Project description:Skeletal tissues including cartilage and bones are characteristic features of vertebrates that are crucial for supporting body morphology and locomotion. Studies mainly in mice have shown that osteoblasts and chondroblasts are supplied from several progenitors in development, growth, and homeostasis. However, developmental origins of osteoblasts and chondroblasts, lineage relationship, progenitor cells, and their differentiation potentials throughout animal life are not seamlessly understood. In this study, we used clonal cell tracking in zebrafish and found that sox9a+ cells are committed to either chondrogenic or osteogenic fates during embryonic stages, and that respective progenies are independently maintained as mesenchymal progenitor pools. Once committed, they never change their lineage identities throughout their lives, even through regeneration. We further showed that osteogenic mesenchymal cells replenish the osteoblast progenitor cells, OPCs, which are the reserved stem cells for osteoblast production during regeneration and homeostasis. Independent mesenchymal progenitors dedicated to produce either chondroblasts or osteoblasts would be important targets for skeletal tissue regeneration.

2023-12-25 | GSE251757 | GEO

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