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Davoodpour, Padideh
Publications (3 of 3) Show all publications
Nilsson Ekdahl, K., Davoodpour, P., Ekstrand-Hammarström, B., Fromell, K., Hamad, O. A., Hong, J., . . . Nilsson, B. (2018). Contact (kallikrein/kinin) system activation in whole human blood induced by low concentrations of α-Fe2O3 nanoparticles.. Nanomedicine: Nanotechnology, Biology and Medicine, 14(3), 735-744
Open this publication in new window or tab >>Contact (kallikrein/kinin) system activation in whole human blood induced by low concentrations of α-Fe2O3 nanoparticles.
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2018 (English)In: Nanomedicine: Nanotechnology, Biology and Medicine, ISSN 1549-9634, E-ISSN 1549-9642, Vol. 14, no 3, p. 735-744Article in journal (Refereed) Published
Abstract [en]

Iron-oxide nanoparticles (NPs) generated by environmental events are likely to represent health problems. alpha-Fe2O3 NPs were synthesized, characterized and tested in a model for toxicity utilizing human whole blood without added anticoagulant. MALDI-TOF of the corona was performed and activation markers for plasma cascade systems (complement, contact and coagulation systems), platelet consumption and release of growth factors, MPO, and chemokine/cytokines from blood cells were analyzed. The coronas formed on the pristine alpha-Fe2O3 NPs contained contact system proteins and they induced massive activation of the contact (kinin/kallikrein) system, as well as thrombin generation, platelet activation, and release of two pro-angiogeneic growth factors: platelet-derived growth factor and vascular endothelial growth factor, whereas complement activation was unaffected. The alpha-Fe2O3 NPs exhibited a noticeable toxicity, with kinin/kallikrein activation, which may be associated with hypotension and long-term angiogenesis in vivo, with implications for cancer, arteriosclerosis and pulmonary disease.

Place, publisher, year, edition, pages
Elsevier, 2018
α-Fe2O3, NPsContact/kallikrein system, Innate immunity
National Category
Immunology in the medical area Nano Technology
urn:nbn:se:uu:diva-343471 (URN)10.1016/j.nano.2017.12.008 (DOI)000429528900010 ()
Swedish Research Council, 2014-3938 2016-2075-5.1 2016-01060 2016-04519EU, FP7, Seventh Framework Programme, 602699AFA Insurance

Joint and equal contribution to senior authorship by Kristina N. Ekdahl, Padideh Davoodpour and Bo Nilsson

Available from: 2018-02-27 Created: 2018-02-27 Last updated: 2019-12-14Bibliographically approved
Davoodpour, P. & Landström, M. (2005). 2-Methoxyestradiol-induced apoptosis in prostate cancer cells requires Smad7. Journal of Biological Chemistry, 280(15), 14773-14779
Open this publication in new window or tab >>2-Methoxyestradiol-induced apoptosis in prostate cancer cells requires Smad7
2005 (English)In: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 280, no 15, p. 14773-14779Article in journal (Refereed) Published
Abstract [en]

Prostate cancer is the second most common cause of death related to cancer in Western society. 2-Methoxyestradiol (2-ME), an endogenous metabolite of estradiol-17beta, inhibits tumor angiogenesis while also exerting potent cytotoxic effects on various cancer cells. 2-ME has been shown to activate the p38 MAPK and JNK pathways and to induce apoptosis in cells, although the underlying molecular mechanisms for this are unknown. Here we report that the expression of Smad7, an adaptor molecule required to activate p38 MAPK in the transforming growth factor beta signaling pathway, is also required for 2-ME-induced p38 activation and apoptosis in human prostate cancer cells (PC-3U). PC-3U/AS-S7 cells stably transfected with an antisense Smad7 construct, or PC-3U cells transiently transfected with short interfering RNA for Smad7, were protected against 2-ME-induced apoptosis. 2-ME-induced apoptosis was found to involve p38 MAPK and JNK, because simultaneous treatments with 2-ME and a specific p38 inhibitor (SB203580) or an inhibitor of JNK (L-JNK1) prevented 2-ME-induced apoptosis. Most interestingly, Smad7 was shown by both antisense and short interfering RNA techniques to affect levels of beta-catenin, which has been implicated previously in the regulation of apoptosis. Moreover, Smad7 was found to be important for the basal expression of Bim, a pro-apoptotic Bcl-2 family member, and for 2-ME-induced expression of Bim. These results suggest that expression of Smad7 is crucial for 2-ME-induced apoptosis in human prostate cancer cells.

National Category
Medical and Health Sciences
urn:nbn:se:uu:diva-93756 (URN)10.1074/jbc.M414470200 (DOI)15708859 (PubMedID)
Available from: 2005-11-17 Created: 2005-11-17 Last updated: 2017-12-14Bibliographically approved
Davoodpour, P., Bergström, M. & Landström, M. (2004). Effects of 2-methoxyestradiol on proliferation, apoptosis and PET-tracer uptake in human prostate cancer cell aggregates. Nuclear Medicine and Biology, 31(7), 867-874
Open this publication in new window or tab >>Effects of 2-methoxyestradiol on proliferation, apoptosis and PET-tracer uptake in human prostate cancer cell aggregates
2004 (English)In: Nuclear Medicine and Biology, ISSN 0969-8051, E-ISSN 1872-9614, Vol. 31, no 7, p. 867-874Article in journal (Refereed) Published
Abstract [en]

The purpose of this study was to investigate the potential use of PET in vivo to record cytotoxic effects of 2-methoxyestradiol (2-ME), an endogenous metabolite of 17beta-estradiol. The anti-proliferative and pro-apoptotic effects of 2-ME on human prostate cancer cell (PC3) aggregates in vitro, were correlated with the uptake of fluoro-deoxy-D-glucose, FMAU and choline labelled with 18F, 11C, or 3H. 2-ME clearly reduced growth of PC3 aggregates and induced apoptosis in a dose-dependent manner. However, the uptake of the putative proliferation markers 11C-FMAU or 3H-choline failed to record the growth inhibitory effects of 2-ME on PC3 cell aggregates. The uptake of 18F-FDG was used as a marker for effects on cellular metabolism and also failed to show any dose-dependent effects in PC3 aggregates. The use of these PET-tracers in vivo is therefore not recommended in order to evaluate the cytotoxic effects of 2-ME on human prostate cancer cells.

Antineoplastic Agents/administration & dosage, Apoptosis/*drug effects, Cell Aggregation/drug effects, Cell Line; Tumor, Cell Proliferation/*drug effects, Comparative Study, Dose-Response Relationship; Drug, Estradiol/*administration & dosage/*analogs & derivatives, Humans, Male, Neoplasm Staging/methods, Positron-Emission Tomography/*methods, Prostatic Neoplasms/drug therapy/*metabolism/pathology/*radionuclide imaging, Radioisotopes/*diagnostic use/*pharmacokinetics, Radiopharmaceuticals/diagnostic use/pharmacokinetics, Reproducibility of Results, Research Support; Non-U.S. Gov't, Sensitivity and Specificity
National Category
Medical and Health Sciences
urn:nbn:se:uu:diva-73054 (URN)10.1016/j.nucmedbio.2004.03.015 (DOI)15464388 (PubMedID)
Available from: 2005-05-31 Created: 2005-05-31 Last updated: 2017-12-14Bibliographically approved

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