Comparison of the chondrosarcoma cell line SW1353 with primary human adult articular chondrocytes with regard to their gene expression profile and reactivity to IL-1beta.
OBJECTIVE
In this study, the human chondrosarcoma cell line SW1353 was investigated by gene expression analysis in order to validate it as an in vitro model for primary human (adult articular) chondrocytes (PHCs).


METHODS
PHCs and SW1353 cells were cultured as high density monolayer cultures with and without 1ng/ml interleukin-1beta (IL-1beta). RNA was isolated and assayed using a custom-made oligonucleotide microarray representing 312 chondrocyte-relevant genes. The expression levels of selected genes were confirmed by real-time polymerase chain reaction and the gene expression profiles of the two cell types, both with and without IL-1beta treatment, were compared.


RESULTS
Overall, gene expression profiling showed only very limited similarities between SW1353 cells and PHCs at the transcriptional level. Similarities were predominantly seen with respect to catabolic effects after IL-1beta treatment. In both cell systems matrix metalloproteinase-1 (MMP-1), MMP-3 and MMP-13 were strongly induced by IL-1beta, without significant induction of MMP-2. IL-6 was also found to be up-regulated by IL-1beta in both cellular models. On the other hand, intercellular mediators such as leukemia inhibitory factor (LIF) and bone morphogenetic protein-2 (BMP-2) were not induced by IL-1beta in SW1353 cells, but significantly up-regulated in PHCs. Bioinformatical analysis identified nuclear factor kappa-B (NFkappaB) as a common transcriptional regulator of IL-1beta induced genes in both SW1353 cells and PHCs, whereas other transcription factors were only found to be relevant for individual cell systems.


CONCLUSIONS
Our data characterize SW1353 cells as a cell line with only a very limited potential to mimic PHCs, though SW1353 cells can be of value to study the induction of protease expression within cells, a phenomenon also seen in chondrocytes.
Gebauer
M
M
Department of Genomic Sciences, Sanofi-Aventis, Frankfurt, FR Germany.
Saas
J
J
Sohler
F
F
Haag
J
J
Söder
S
S
Pieper
M
M
Bartnik
E
E
Beninga
J
J
Zimmer
R
R
Aigner
T
T
D000368:Aged; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins / Q000235:genetics; D002358:Cartilage, Articular / Q000166:cytology*; D045744:Cell Line, Tumor; D019902:Chondrocytes / Q000502:physiology*; D015536:Down-Regulation / Q000235:genetics; D005109:Extracellular Matrix / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation / Q000235:genetics*; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics*; D015850:Interleukin-6 / Q000235:genetics; D053605:Leukemia Inhibitory Factor; D008297:Male; D020782:Matrix Metalloproteinases / Q000032:analysis; D008875:Middle Aged; D008954:Models, Biological; D016328:NF-kappa B / Q000235:genetics; D020411:Oligonucleotide Array Sequence Analysis; D016133:Polymerase Chain Reaction / Q000379:methods; D014157:Transcription Factors / Q000032:analysis; D016212:Transforming Growth Factor beta / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics
C525718:BMP2 protein, human; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins; D007375:Interleukin-1; D015850:Interleukin-6; C507837:LIF protein, human; D053605:Leukemia Inhibitory Factor; D016328:NF-kappa B; D014157:Transcription Factors; D016212:Transforming Growth Factor beta; D020782:Matrix Metalloproteinases