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ID 32996
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Author
Moritani, Norifumi H
Kubota, Satoshi Kakenhi
Sugahara, Toshio
Abstract

Background: The chondrosarcoma-derived HCS-2/8 has been known to be an excellent model of human articular chondrocytes. By mimicking the arthritic conditions through the treatment of HCS-2/8 cells with cytokines, we estimated the gene expression response of ccn1 and ccn2 during the course of joint inflammation in vitro.
Results: In order to mimic the initiation of inflammation, HCS-2/8 cells were treated with tumor necrosis factor (TNF)-α. To induce pro-inflammatory or reparative responses, TGF-β was employed. Effects of an anti-inflammatory glucocorticoid were also evaluated. After stimulation, expression levels of ccn1 and ccn2 were quantitatively analyzed. Surprisingly, not only ccn2, but also ccn1 expression was repressed upon TNF-α stimulation, whereas both mRNAs were uniformly induced by transforming growth factor (TGF)-β and a glucocorticoid.
Conclusion: These results describing the same response during the course of inflammation suggest similar and co-operative roles of these 2 ccn family members in the course of arthritis.

Note
Digital Object Identifier:10.1186/1478-811X-3-6
Published with permission from the copyright holder. This is the institute's copy, as published in Cell Communication and Signaling, Volume 3, 15 April 2005, Article number 6.
Publisher URL:http://dx.doi.org/10.1186/1478-811X-3-6
Copyright © 2005 Moritani et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Published Date
2005-04-15
Publication Title
Cell Communication and Signaling
Volume
volume3
Issue
issue1
Publisher
BioMed Central
NCID
AA12050544
Content Type
Journal Article
language
英語
Copyright Holders
Moritani et al; licensee BioMed Central Ltd.
File Version
publisher
Refereed
True
DOI
PubMed ID
Submission Path
biology_general/1