Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide analysis of cartilage gene expression in response to cartilage-specific ablation of Site-1 protease (Mbtps1) in mice (S1Pcko mice)

ABSTRACT: Analysis of differential gene expression in chondrocytes due to S1P ablation in mice. The hypothesis tested in this study was that ablation of S1P in mice would result in differential gene expression in chondrocytes that may be responsible for the S1Pcko phenotype. The chondroepiphyseal cartilage from the tip of appendicular bones such as femur, tibia, humerus, radius, ulna were harvested from E16.5 wild type (WT) and S1Pcko embryos. In addition, the appendicular bones and calvarium from E16.5 WT and S1Pcko embryos also were harvested and processed for total RNA without removing the chondroepiphyseal cartilage. The chondroepiphyseal cartilage and bones were rolled on Whatman Filter paper to remove muscle and blood vessels, and total RNA was extracted, labeled, hybridized on Illumina Mouse WG-6 v1.1 and analyzed to identify genes that were differentially expressed in the S1Pcko skeletal elements when compared to WT.

ORGANISM(S): Mus musculus

SUBMITTER: Debabrata Patra

PROVIDER: E-GEOD-55577 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Endochondral ossification is the process by which the appendicular skeleton, facial bones, vertebrae and medial clavicles are formed and relies on the tight control of chondrocyte maturation. Fibroblast growth factor receptor (FGFR)3 plays a role in bone development and maintenance and belongs to a family of proteins which differ in their ligand affinities and tissue distribution. Activating mutations of the FGFR3 gene lead to craniosynostosis and multiple types of skeletal dysplasia with varying degrees of severity: thanatophoric dysplasia (TD), achondroplasia and hypochondroplasia. Despite progress in the characterization of FGFR3-mediated regulation of cartilage development, many aspects remain unclear. The aim and the novelty of our study was to examine whole gene expression differences occurring in primary human chondrocytes isolated from normal cartilage or pathological cartilage from TD-affected fetuses, using Affymetrix technology. The phenotype of the primary cells was confirmed by the high expression of chondrocytic markers. Altered expression of genes associated with many cellular processes was observed, including cell growth and proliferation, cell cycle, cell adhesion, cell motility, metabolic pathways, signal transduction, cell cycle process and cell signaling. Most of the cell cycle process genes were down-regulated and consisted of genes involved in cell cycle progression, DNA biosynthesis, spindle dynamics and cytokinesis. About eight percent of all modulated genes were found to impact extracellular matrix (ECM) structure and turnover, especially glycosaminoglycan (GAG) and proteoglycan biosynthesis and sulfation. Altogether, the gene expression analyses provide new insight into the consequences of FGFR3 mutations in cell cycle regulation, onset of pre-hypertrophic differentiation and concomitant metabolism changes. Moreover, impaired motility and ECM properties may also provide clues about growth plate disorganization. These results also suggest that many signaling pathways may be directly or indirectly altered by FGFR3 and confirm the crucial role of FGFR3 in the control of growth plate development.

Dataset Information

Genome-wide analysis of cartilage gene expression in response to cartilage-specific ablation of Site-1 protease (Mbtps1) in mice (S1Pcko mice)

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