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Effect of transforming growth factor-beta on calcium homeostasis inprostate carcinoma cells.
Ludwiginstitutet för Cancerforskning.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Cell Biology.
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2003 (English)In: Biochem Biophys Res Commun, Vol. 304, 643- p.Article in journal (Refereed) Published
Abstract [en]

Ca(2+) plays a fundamental role in the control of a variety of cellular functions, in particular, in energy metabolism and apoptosis. In this study, we show that TGF-beta at concentrations of 0.1-1.0 ng/ml transiently increases the level of intracellular Ca(2+) ([Ca(2+)](in)) in human prostate carcinoma, PC-3U, cells. Experiments with mitochondrial inhibitors (oligomycin and antimycin A) and an inhibitor of endoplasmic reticulum Ca(2+) uptake (BHQ) implied that the effect of TGF-beta1 was due to an effect on the mitochondria. TGF-beta1 treatment resulted in a decrease in ATP synthesis and to a depolarisation, leading to a release of Ca(2+) from mitochondria and decreased activity of the Ca(2+) pumps. Analysis of the mitochondria within the PC-3U cells by polarography and membrane potential-sensitive dye (Rhodamine 123) confirmed that under these experimental conditions, TGF-beta1 inhibited ATP synthesis and depolarised the mitochondria. The results implicate that TGF-beta1 affects the function of the mitochondria and may be of significance for the understanding of the proapoptotic effect of TGF-beta1 in these cells.

Place, publisher, year, edition, pages
2003. Vol. 304, 643- p.
URN: urn:nbn:se:uu:diva-64061PubMedID: 12727202OAI: oai:DiVA.org:uu-64061DiVA: diva2:91972
Available from: 2005-06-14 Created: 2005-06-14 Last updated: 2011-01-13

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Grapengiesser, EvaHeldin, Carl-HenrikAspenström, Pontus
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