Normal proliferation and differentiation of Hoxc-8 transgenic chondrocytes in vitro

@article{Cormier2003NormalPA,
  title={Normal proliferation and differentiation of Hoxc-8 transgenic chondrocytes in vitro},
  author={Stephania A. Cormier and Maria Alice Rostom Mello and Claudia Kappen},
  journal={BMC Developmental Biology},
  year={2003},
  volume={3},
  pages={4 - 4},
  url={https://api.semanticscholar.org/CorpusID:1629122}
}
In vitro analysis of cartilage-producing cells from Hoxc-8 transgenic mice provides evidence that the cellular phenotype induced by HoxC-8 overexpression in vivo is reversible in vitro, validating in vitro approaches for studies of Hox genes in the regulation of endochondral ossification.
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25 Citations
Background Citations
6
Methods Citations
8
Results Citations
1

25 Citations

Morpholino-mediated knockdown in primary chondrocytes implicates Hoxc8 in regulation of cell cycle progression.

Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice

The differences in repertoires of altered gene expression between the 2 transgenic conditions suggest that the molecular mechanisms underlying the cartilage defects may be different in both transgenic paradigms, despite apparently similar phenotypes.

Expression of folate pathway genes in the cartilage of Hoxd4 and Hoxc8 transgenic mice.

This study shows that the Hox transgenes produce overexpression of Hoxd4 and Hoxc8 in primary chondrocytes from perinatal transgenic mice, but no differences were found in expression levels of the folate pathway genes in transgenic cells compared to littermate controls.

Unbiased transcriptomic analysis of chondrocyte differentiation in a high-density cell culture model

The overarching goal of this study was to characterize the molecular pathways involved in cartilage differentiation and maturation, and to enable a comprehensive appraisal of distinctions between common in vitro models for Cartilage differentiation, and of differences in their molecular resemblance to cartilage formation in vivo.

Expression of Cartilage Developmental Genes in Hoxc8- and Hoxd4-Transgenic Mice

It is suggested that both transcription factors affect cartilage maturation through different molecular mechanisms, and provide the basis for future studies into the role of these genes and possible interactions in pathogenesis of cartilage defects in Hoxc8- and Hoxd4-transgenic mice.

Microarray analyses of gene expression during chondrocyte differentiation identifies novel regulators of hypertrophy.

Overexpression of Rgs2 in the chondrogenic cell line ATDC5 resulted in accelerated hypertrophic differentiation, thus providing functional validation of microarray data and providing novel information on the temporal expression of molecules regulating endochondral bone development.

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Hox genes and mesenchymal stem cells

It is shown that the elements that are responsible for expression of HOXA genes in hematopoietic cells are most likely located at a remote position outside the cluster, which could potentially lead to the identification of these elusive elements.

Control of collagen production in mouse chondrocytes by using a combination of bone morphogenetic protein-2 and small interfering RNA targeting Col1a1 for hydrogel-based tissue-engineered cartilage.

A new strategy for authorizing the recovery of the differentiated status of the chondrocytes after their amplification on plastic is proposed and the BMP-2/Col1a1 siRNA combination is effective in reinitializing correct production and assembly of the cartilage-characteristic matrix in agarose hydrogel, without production of type I collagen.

Thyroid hormone-stimulated differentiation of primary rib chondrocytes in vitro requires thyroid hormone receptor beta.

It is indicated that T(3)-stimulated differentiation of primary rib chondrocytes in vitro requires TRbeta and suggest that the TRbeta1 isoform mediates important T( 3) actions in mouse rib chonds in vivo.

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