Ablation of collagen IX and COMP disrupts epiphyseal cartilage architecture

Blumbach, Katrin; Niehoff, Anja; Paulsson, Mats; Zaucke, Frank

doi:10.1016/j.matbio.2007.11.007

Cited by 48 publications

(51 citation statements)

References 51 publications

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“…We then used this approach to assess the growth plate composition of Col9a1-deficient mice that display severe growth plate abnormalities with large hypocellular areas and a widening of the circumferences of the bone. (25,37) Quantitative flow cytometry analysis of growth plate cell suspensions from three 12-or 13-day-old mutant mice (Fig. 6B) showed that these mice contain a significantly higher proportion of proliferative cells (ratio 12 days: [P/PH-H] ¼ 7 to 8; 13 days: [P/PH-H] ¼ 4 to 5) compared with wild-type mice (Fig.…”

Section: Assessment Of the Growth Plate Composition During Developmentmentioning

confidence: 99%

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

Belluoccio¹,

Etich²,

Rosenbaum³

et al. 2010

Journal of Bone and Mineral Research

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Axial growth of long bones occurs through a coordinated process of growth plate chondrocyte proliferation and differentiation. This maturation of chondrocytes is reflected in a zonal change in gene expression and cell morphology from resting to proliferative, prehypertrophic, and hypertrophic chondrocytes of the growth plate followed by ossification. A major experimental limitation in understanding growth plate biology and pathophysiology is the lack of a robust technique to isolate cells from the different zones, particularly from small animals. Here, we report on a new strategy for separating distinct chondrocyte populations from mouse growth plates. By transcriptome profiling of microdissected zones of growth plates, we identified novel, zone-specific cell surface markers and used these for flow cytometry and immunomagnetic cell separation to quantify, enrich, and characterize chondrocytes populations with respect to their differentiation status. This approach provides a novel platform to study cartilage development and characterize mouse growth plate chondrocytes to reveal unique cellular phenotypes of the distinct subpopulations within the growth plate. ß

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Section: Assessment Of the Growth Plate Composition During Developmentmentioning

confidence: 99%

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

Belluoccio¹,

Etich²,

Rosenbaum³

et al. 2010

Journal of Bone and Mineral Research

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“…COMP interacts with multiple other cartilage matrix components, including type I, II, and IX collagens (10), proteoglycans such as aggrecan (11), non-collagenous matrix proteins such as fibronectin (12), and matrilins (13), as well as with glycosaminoglycans and heparin (11,14). The repeated modular structure of COMP is critically important for its function as a "bridge" that assembles multiple extracellular matrix components (9); for example, the COMP pentamer (but not monomeric COMP) simultaneously binds several free collagen molecules to accelerate collagen fibrillogenesis (15).…”

Section: Mature Cartilage Oligomeric Matrix Protein (Comp)mentioning

confidence: 99%

Enhanced Activity of Transforming Growth Factor β1 (TGF-β1) Bound to Cartilage Oligomeric Matrix Protein

Haudenschild

Hong

Yik

et al. 2011

Journal of Biological Chemistry

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“…A potential role for cell-matrix adhesion is further supported by altered growth plate structure in mouse mutants of cell-matrix interaction molecules (see Table S2 in the supplementary material). However, of these mutants, only loss-of-function of integrin β1 (Aszodi et al, 2003) and ColIX (Blumbach et al, 2008;Dreier et al, 2008) display substantial loss of proliferative chondrocyte structure. Despite similarities to the phenotypes we describe, differences such as decreased cell proliferation and hypocellularity in cell adhesion mutants suggest that the polarity defects described in the present studies might not be solely due to altered cell-matrix interactions.…”

Section: Research Articlementioning

confidence: 99%

Noncanonical frizzled signaling regulates cell polarity of growth plate chondrocytes

2009

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Bone growth is driven by cell proliferation and the subsequent hypertrophy of chondrocytes arranged in columns of discoid cells that resemble stacks of coins. However, the molecular mechanisms that direct column formation and the importance of columnar organization to bone morphogenesis are not known. Here,we show in chick that discoid proliferative chondrocytes orient the division plane to generate daughter cells that are initially displaced laterally and then intercalate into the column. Downregulation of frizzled (Fzd) signaling alters the dimensions of long bones and produces cell-autonomous changes in proliferative chondrocyte organization characterized by arbitrary division planes and altered cell stacking. These defects are phenocopied by disruption of noncanonical effector pathways but not by inhibitors of canonical Fzd signaling. These findings demonstrate that the regulation of cell polarity and cell arrangement by noncanonical Fzd signaling plays important roles in generating the unique morphological characteristics that shape individual cartilage elements.

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Ablation of collagen IX and COMP disrupts epiphyseal cartilage architecture

Cited by 48 publications

References 51 publications

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

Enhanced Activity of Transforming Growth Factor β1 (TGF-β1) Bound to Cartilage Oligomeric Matrix Protein

Noncanonical frizzled signaling regulates cell polarity of growth plate chondrocytes

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