Expression of matrix proteins during the development of mineralized tissues

Sommer, Beatrice; Bickel, M.; Hofstetter, Willy; Wetterwald, Antoinette

doi:10.1016/s8756-3282(96)00218-9

Cited by 131 publications

(104 citation statements)

References 36 publications

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“…5A). During endochondral ossification, chondrocytes differentiate into hypertrophic chondrocytes and express osteopontin, which is not normally expressed by mature human articular chondrocytes [7,19,36,49]. Furthermore, several reports have confirmed that osteopontin expression is increased, both at the mRNA and protein level, in human OA [27,41].…”

Section: Discussionmentioning

confidence: 99%

Intrajoint comparisons of gene expression patterns in human osteoarthritis suggest a change in chondrocyte phenotype

Yagi

McBurney

Laverty

et al. 2005

Journal Orthopaedic Research

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Osteoarthritis (OA) is a degenerative cartilage disease with varying degrees of severity within a given joint. The purpose of this study was to define a sampling procedure for comparing human minimal and advanced OA cartilage in the same patient and to determine basic patterns of gene expression in these regions. A specific hypothesis under study was that the expression level of Bcl-2 would correlate with sox9 and aggrecan mRNA expression in vivo as has been demonstrated in vitro. Femoral condylar advanced OA cartilage was located within 1 cm of overt lesions, and minimal cartilage was taken from areas with no obvious surface defects. Histological sections were scored for disease severity and chondroitin sulfate and hydroxyproline content was determined. The expression level of nine specific genes (aggrecan, collagen type 11, Bcl-2, sox9, Link protein, osteopontin, and MMP-13, -3, and -9) was determined by quantitative real time PCR. The scores for fibrillation, chondrocyte cloning, and proteoglycan depletion were significantly different between advanced and minimal OA cartilage. The advanced OA cartilage had significantly less chondroitin sulfate than the minimal OA cartilage. Osteopontin mRNA expression showed a 3.6-fold increase in advanced compared to minimal OA cartilage. In contrast, the level of mRNA coding for aggrecan, link protein, Bcl-2, sox9 and MMP-3, -9, -13 were all decreased in advanced compared to minimal cartilage in the majority of the patients studied. Collagen type I1 mRNA expression displayed a wide-range of variation. A statistically significant correlation was observed both between Bcl-2 and sox9 mRNA level, and between Bcl-2 and aggrecan mRNA expression. The patient matched comparison of minimal and advanced OA cartilage revealed differences in cellular and tissue characteristics, and changes in gene expression that may be involved in OA progression. In addition, Bcl-2 may also play a role in regulating the expression of aggrecan through sox9 in vivo as well as in vitro.

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Section: Discussionmentioning

confidence: 99%

Intrajoint comparisons of gene expression patterns in human osteoarthritis suggest a change in chondrocyte phenotype

Yagi

McBurney

Laverty

et al. 2005

Journal Orthopaedic Research

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“…Discrepancies between protein and mRNA expression have been previously noted for several molecules and are generally believed to result from differences in, e.g., the stability of the mRNA/protein reflecting post-transcriptional/post-translational modulation, differences between synthesizing cells vs target cells, and/or differences in detection limits of probes and antibodies used. The localization of STC1 protein in cartilaginous tissue appears to correspond to the differentiation stage, during which chondrocytes start to mineralize their extracellular matrix (Alini et al 1994;Sommer et al 1996). The cell surface receptor for gibbon ape leukemia virus (Glvr-1/PiT1), the Type III sodium-dependent phosphate transporter/retrovirus receptor gene, has also been reported to be localized to the same zone where it may regulate inorganic phosphate (P i ) uptake in osteogenic cells and contribute to bone mineralization (Palmer et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Stanniocalcin 1 (STC1) Protein and mRNA Are Developmentally Regulated During Embryonic Mouse Osteogenesis: the Potential of STC1 as an Autocrine/Paracrine Factor for Osteoblast Development and Bone Formation

Yoshiko

Aubin

Maeda

2002

J Histochem Cytochem.

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S U M M A R Y STC1, a mammalian homologue of stanniocalcin (STC) which plays a major role in calcium/phosphate homeostasis in fish, has been recently isolated. We have characterized the spatiotemporal distribution of STC1 mRNA and protein during mouse embryonic development generally and osteogenesis specifically. Northern blotting analysis of whole embryos showed that STC1 mRNA is highly and differentially expressed during embryogenesis. By in situ hybridization, STC1 mRNA was detected early in mesenchymal condensations and was then found to be highly expressed in perichondrial cells, periosteal cells, and then osteoblasts during endochondral bone formation. In bones forming by intramembranous ossification, STC1 mRNA was not detected until osteogenic cells appeared. The cellular distribution of STC1 protein closely corresponded to that of its mRNA, but the protein was also detected in hypertrophic chondrocytes. In the MC3T3-E1 osteogenic cell model, STC1 protein and mRNA were detectable throughout proliferation and differentiation stages but levels were relatively higher late during nodule formation/mineralization phases. For comparison, STC1 mRNA was also found in epithelial cells of both embryonic and adult intestine that had not previously been described among tissues responsive to calcium/phosphate transport. These results suggest that STC1 is expressed in a time-and cellspecific manner and may play an autocrine/paracrine role during osteoblast development and bone formation.

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“…Development 136 (20) 1993; Sommer et al, 1996). Thus, gpi-anchored proteins are not required for skeletal patterning or osteoblast formation, but might have additional roles in osteoblast cells.…”

Section: Research Articlementioning

confidence: 99%

Convergent extension movements in growth plate chondrocytes require gpi-anchored cell surface proteins

Ahrens

Jiang

et al. 2009

Development

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Proteins that are localized to the cell surface via glycosylphosphatidylinositol (gpi) anchors have been proposed to regulate cell signaling and cell adhesion events involved in tissue patterning. Conditional deletion of Piga, which encodes the catalytic subunit of an essential enzyme in the gpi-biosynthetic pathway, in the lateral plate mesoderm results in normally patterned limbs that display chondrodysplasia. Analysis of mutant and mosaic Piga cartilage revealed two independent cell autonomous defects. First, loss of Piga function interferes with signal reception by chondrocytes as evidenced by delayed maturation. Second, the proliferative chondrocytes, although present, fail to flatten and arrange into columns. We present evidence that the abnormal organization of mutant proliferative chondrocytes results from errors in cell intercalation. Collectively, our data suggest that the distinct morphological features of the proliferative chondrocytes result from a convergent extension-like process that is regulated independently of chondrocyte maturation.

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Expression of matrix proteins during the development of mineralized tissues

Cited by 131 publications

References 36 publications

Intrajoint comparisons of gene expression patterns in human osteoarthritis suggest a change in chondrocyte phenotype

Intrajoint comparisons of gene expression patterns in human osteoarthritis suggest a change in chondrocyte phenotype

Stanniocalcin 1 (STC1) Protein and mRNA Are Developmentally Regulated During Embryonic Mouse Osteogenesis: the Potential of STC1 as an Autocrine/Paracrine Factor for Osteoblast Development and Bone Formation

Convergent extension movements in growth plate chondrocytes require gpi-anchored cell surface proteins

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