Meeting details menu

Meeting Authors
Meeting Abstracts
Keynote lectures
Oral communications
Poster presentations
Special symposia
Other

Acta Physiologica Congress

Back

Acta Physiologica 2011; Volume 201, Supplement 682
The 90th Annual Meeting of The German Physiological Society
3/26/2011-3/29/2011
Regensburg, Germany


INFLUENCE OF OCHRATOXIN A ON GENE EXPRESSION IN PRIMARY HUMAN PROXIMAL TUBULE CELLS
Abstract number: P129

*Hennemeier1 I., Gekle1 M., Schwerdt1 G.

Ochratoxin A (OTA), a mycotoxin produced by different Aspergillus and Penicillium species, is a ubiquitous contaminant of food, which has both nephrotoxic and carcinogenic potential. The underlying changes of gene expression responsible for nephrotoxicity and cancerogenity of OTA are still unknown. Therefore, the effect of nanomolar OTA concentrations on gene expression was analyzed in human kidney proximal tubule cells (RPTEC) in primary culture. Cells were incubated with 10 nM OTA for 14 days, RNA was isolated and the effect of OTA was examined using different pathway specific RT² Profiler PCR Arrays. The PCR array data indicate that prolonged OTA exposure influences Wnt-signaling by altering the expression of genes involved in this pathway (up-regulation: APC, WISP1, WT1; down-regulation: TCF7). Wnt-signaling is known to be essential in embryogenesis and also kidney development. A disruption of this pathway can trigger cancerogenesis. Furthermore, OTA increases the expression of genes that are involved in inflammatory processes (TNF-a, COX2 and NFkB) and thus cause fibrotic changes in renal tissue. In summary, a long-term exposure of human primary kidney cells with an OTA concentration detectable in human renal tissue changes the expression of genes that are involved in both Wnt-signaling and inflammation. These findings allow a new perspective on how OTA leads to kidney damage. (This work was supported by the Deutsche Forschungsgemeinschaft; GE 905/12-2)

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 201, Supplement 682 :P129

Our site uses cookies to improve your experience.You can find out more about our use of cookies in our standard cookie policy, including instructions on how to reject and delete cookies if you wish to do so.

By continuing to browse this site you agree to us using cookies as described in our standard cookie policy .

CLOSE