Gene expression in TGFbeta-induced epithelial cell differentiation in a three-dimensional intestinal epithelial cell differentiation model

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dc.contributor.author Juuti-Uusitalo, Kati M
dc.contributor.author Kaukinen, Katri
dc.contributor.author Mäki, Markku
dc.contributor.author Tuimala, Jarno
dc.contributor.author Kainulainen, Heikki
dc.date.accessioned 2012-11-22T09:25:16Z
dc.date.available 2012-11-22T09:25:16Z
dc.date.issued 2006 fi
dc.identifier.citation Juuti-Uusitalo, K., Kaukinen, K., Mäki, M., Tuimala, J., & Kainulainen, H. (2006). Gene expression in TGFbeta-induced epithelial cell differentiation in a three-dimensional intestinal epithelial cell differentiation model. BMC Genomics, 7:279. doi:10.1186/1471-2164-7-279 fi
dc.identifier.uri http://dx.doi.org/10.1186/1471-2164-7-279
dc.identifier.uri http://hdl.handle.net/123456789/40406
dc.description.abstract Background. The TGFβ1-induced signal transduction processes involved in growth and differentiation are only partly known. The three-dimensional epithelial differentiation model, in which T84 epithelial cells are induced to differentiate either with TGFβ1 or IMR-90 mesenchymal cell-secreted soluble factors, is previously shown to model epithelial cell differentiation seen in intestine. That model has not been used for large scale gene expression studies, such as microarray method. Therefore the gene expression changes were studied in undifferentiated and differentiated three-dimensional T84 cultures with cDNA microarray method in order to study the molecular changes and find new players in epithelial cell differentiation. Results. The expression of 372 genes out of 5188 arrayed sequences was significantly altered, and 47 of them were altered by both mediators. The data were validated and the altered genes are presented in ontology classes. For the genes tested the expressions in protein level were in accordance with the mRNA results. We also found 194 genes with no known function to be potentially important in epithelial cell differentiation. The mRNA expression changes induced by TGFβ1 were bigger than changes induced by soluble factors secreted by IMR-90 mesenchymal cells. The gene expression data was depicted in already known signaling pathway routes. Conclusion. Our results reveal potential new signaling pathways and several new genes affected by TGFβ in epithelial cell differentiation. The differentiation induced by TGFβ1 appears to be more potent than the differentiation induced by mesenchymal cells. This study indicates that our cell culture model is a suitable tool in studying regulatory mechanisms during epithelial cell differentiation in intestine. Furthermore the present results indicate that our model is a good tool for finding new players acting in the differentiation of epithelial cells. fi
dc.language.iso eng
dc.publisher BioMed Central (BMC)
dc.relation.ispartofseries BMC Genomics
dc.relation.ispartofseries 1471-2164
dc.rights © 2006 Juuti-Uusitalo 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.
dc.rights.uri http://creativecommons.org/licenses/by/2.0
dc.subject.other epiteelisolu
dc.subject.other erilaistuminen
dc.subject.other TGF-beta
dc.subject.other geenilastu
dc.subject.other geenien ilmeneminen
dc.subject.other epithelial cell
dc.subject.other differentiation
dc.subject.other TGB-beta
dc.subject.other microarray
dc.subject.other gene expression
dc.title Gene expression in TGFbeta-induced epithelial cell differentiation in a three-dimensional intestinal epithelial cell differentiation model fi
dc.type Article en
dc.contributor.laitos Liikuntabiologian laitos fi
dc.contributor.laitos Department of Biology of Physical Activity en
dc.type.uri http://purl.org/eprint/type/JournalArticle
dc.identifier.doi 10.1186/1471-2164-7-279
dc.date.updated 2012-11-15T14:59:38Z
dc.description.version Published version
eprint.status http://purl.org/eprint/type/status/PeerReviewed

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