oru.sePublications
Change search
Link to record
Permanent link

Direct link
BETA
Sundström, Birgitta E.ORCID iD iconorcid.org/0000-0001-9302-2396
Alternative names
Publications (4 of 4) Show all publications
Rendel, F., Fjaeraa Alfredsson, C., Bornehag, C.-G., Sundström, B. E. & Nånberg, E. (2017). Effects of Di-Isononyl Phthalate on Neuropeptide Y Expression in Differentiating Human Neuronal Cells. Basic & Clinical Pharmacology & Toxicology, 120(3), 218-323
Open this publication in new window or tab >>Effects of Di-Isononyl Phthalate on Neuropeptide Y Expression in Differentiating Human Neuronal Cells
Show others...
2017 (English)In: Basic & Clinical Pharmacology & Toxicology, ISSN 1742-7835, E-ISSN 1742-7843, Vol. 120, no 3, p. 218-323Article in journal (Refereed) Published
Abstract [en]

Neuropeptide Y (NPY) is an abundant neuropeptide in the mammalian brain important for behavioural consequences of stress and energy metabolism. We have addressed possible effects of the phthalate DiNP on NPY expression in human SH‐SY5Y cells, a neuronal in vitro differentiation model. Pico‐ to nanomolar doses of DiNP and its metabolite MiNP resulted in decreased NPY mRNA and peptide expression in retinoid‐differentiated cells. Thus, dys‐regulated NPY may be an adverse outcome for exposure to low doses of DiNP in human beings.

Place, publisher, year, edition, pages
Blackwell Publishing, 2017
Keywords
phthlate, DiNP, MiNP, NPY, SH-SY5Y neuroblastoma cells
National Category
Medical and Health Sciences Cell and Molecular Biology
Research subject
Biomedical Sciences; Biomedical Sciences
Identifiers
urn:nbn:se:oru:diva-79055 (URN)10.1111/bcpt.12670 (DOI)000394538600016 ()27625336 (PubMedID)2-s2.0-85009476073 (Scopus ID)
Note

This work was financially supported by The County Council of Värmland.

Retraction

The above article, published online on 13 September 2016 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor in Chief, Kim Brøsen, the Nordic Association for the Publication of BCPT and John Wiley & Sons Ltd. The retraction has been agreed following an investigation into the accuracy of the data acquisition conducted by Karlstad University into the accuracy of the data acquisition, which concluded that manipulation had taken place during tests performed on an ELISA equipment in order to achieve a preferred result.

Available from: 2016-09-05 Created: 2020-01-17 Last updated: 2020-02-03Bibliographically approved
Fjæraa Alfredsson, C., Rendel, F., Liang, Q.-L., Sundström, B. E. & Nånberg, E. (2015). Altered sensitivity to ellagic acid in neuroblastoma cells undergoing differentiation with 12-0-tetradecanoylphorbol-13-acetate and all-trans retinoic acid. Biomedicine and Pharmacotherapy, 76, 39-45
Open this publication in new window or tab >>Altered sensitivity to ellagic acid in neuroblastoma cells undergoing differentiation with 12-0-tetradecanoylphorbol-13-acetate and all-trans retinoic acid
Show others...
2015 (English)In: Biomedicine and Pharmacotherapy, ISSN 0753-3322, E-ISSN 1950-6007, Vol. 76, p. 39-45Article in journal (Refereed) Published
Abstract [en]

Ellagic acid has previously been reported to induce reduced proliferation and activation of apoptosis in several tumor cell lines including our own previous data from non-differentiated human neuroblastoma SH-SY5Y cells. The aim of this study was now to investigate if in vitro differentiation with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate or the vitamin A derivative all-trans retinoic acid altered the sensitivity to ellagic acid in SH-SY5Y cells. The methods used were cell counting and LDH-assay for evaluation of cell number and cell death, flow cytometric analysis of SubG(1)-and TUNEL-analysis for apoptosis and western blot for expression of apoptosis-associated proteins. In vitro differentiation was shown to reduce the sensitivity to ellagic acid with respect to cell detachment, loss of viability and activation of apoptosis. The protective effect was phenotype-specific and most prominent in all-trans retinoic acid-differentiated cultures. Differentiation-dependent up-regulation of Bcl-2 and integrin expression is introduced as possible protective mechanisms. The presented data also point to a positive correlation between proliferative activity and sensitivity to ellagic-acid-induced cell detachment. In conclusion, the presented data emphasize the need to consider degree of neuronal differentiation and phenotype of neuroblastoma cells when discussing a potential pharmaceutical application of ellagic acid in tumor treatment.

Place, publisher, year, edition, pages
Elsevier, 2015
Keywords
Ellagic acid, Cell adhesion, Apoptosis, Neuroblastoma, Differentiation
National Category
Basic Medicine Cell and Molecular Biology
Research subject
Biomedical Sciences
Identifiers
urn:nbn:se:oru:diva-79030 (URN)10.1016/j.biopha.2015.10.008 (DOI)000367541500007 ()26653548 (PubMedID)2-s2.0-84949206850 (Scopus ID)
Funder
The Royal Swedish Academy of Sciences
Note

This work was financially supported by The County Council of Värmland, The Swedish Childrens Cancer Society and The Royal Swedish Academy of Sciences.

Available from: 2013-10-24 Created: 2020-01-17 Last updated: 2020-01-27Bibliographically approved
Fjæraa Alfredsson, C., Ding, M., Liang, Q.-L., Sundström, B. & Nånberg, E. (2014). Ellagic acid induces a dose- and time-dependent depolarization of mitochondria and activation of caspase-9 and -3 in human neuroblastoma cells. Biomedicine and Pharmacotherapy, 68(1), 129-135
Open this publication in new window or tab >>Ellagic acid induces a dose- and time-dependent depolarization of mitochondria and activation of caspase-9 and -3 in human neuroblastoma cells
Show others...
2014 (English)In: Biomedicine and Pharmacotherapy, ISSN 0753-3322, E-ISSN 1950-6007, Vol. 68, no 1, p. 129-135Article in journal (Refereed) Published
Abstract [en]

The polyphenol ellagic acid is found in many natural food sources and has been proposed as a candidate compound for clinical applications due to its anti-oxidative capacity and as a potential anti-tumorigenic compound. The objective of the present study was to evaluate the sensitivity to and possible apoptosis mechanism induced by ellagic acid in neuronal tumor cells. As a model the human neuroblastoma SH-SY5Y cell line was used. The methods applied were bright field and phase contrast microscopy, XTT- and LDH-assays, western blot, and flow cytometric analysis of DNA degradation and mitochondrial membrane potential. Ellagic acid treatment was found to induce a reduction in cell number preceded by alterations of the mitochondrial membrane potential and activation of caspase-9 and -3, DNA-fragmentation and cell death by apoptosis. The apoptotic cell death studied was not due to anoikis since it was significant in the adherent fraction of the cells. We conclude that ellagic acid induces dose- and time-dependent apoptosis, at least partly by the mitochondrial pathway, in an embryonal neuronal tumor cell system. This finding is in agreement with previously reported data on adult carcinoma cells thus suggesting a more general effect of ellagic acid on tumor cells.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Ellagic acid, Caspase, Mitochondrial membrane potential
National Category
Medical and Health Sciences Pharmacology and Toxicology
Identifiers
urn:nbn:se:oru:diva-79029 (URN)10.1016/j.biopha.2013.08.010 (DOI)000332448400019 ()24051122 (PubMedID)2-s2.0-84895072497 (Scopus ID)
Note

This work was financially supported by The County Council of Värmland and The Swedish Childrens Cancer Society.

Available from: 2013-10-17 Created: 2020-01-17 Last updated: 2020-01-27Bibliographically approved
Fjæraa Alfredsson, C., Rendel, F., Sundström, B. E. & Nånberg, E.Proliferation in morphologically differentiated SH-SY5Y human neuroblastoma cells.
Open this publication in new window or tab >>Proliferation in morphologically differentiated SH-SY5Y human neuroblastoma cells
(English)Manuscript (preprint) (Other academic)
National Category
Medical and Health Sciences Cell and Molecular Biology
Research subject
Biomedical Sciences
Identifiers
urn:nbn:se:oru:diva-79031 (URN)
Available from: 2013-10-24 Created: 2020-01-17 Last updated: 2020-02-03Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-9302-2396

Search in DiVA

Show all publications