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Petersson, Stina
Publications (6 of 6) Show all publications
Carlström, M., Ekman, A.-K., Petersson, S., Söderkvist, P. & Enerbäck, C. (2012). Genetic support for the role of the NLRP3 inflammasome in psoriasis susceptibility. Experimental dermatology, 21(12), 932-937
Open this publication in new window or tab >>Genetic support for the role of the NLRP3 inflammasome in psoriasis susceptibility
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2012 (English)In: Experimental dermatology, ISSN 0906-6705, E-ISSN 1600-0625, Vol. 21, no 12, p. 932-937Article in journal (Refereed) Published
Abstract [en]

NACHT leucine-rich repeat- and PYD-containing (NLRP)3 protein controls the inflammasome by regulating caspase-1 activity and interleukin (IL)-1 beta processing. The contribution of IL-1 beta in the pathogenesis of psoriasis is well recognized. Polymorphisms in NLRP3 and caspase recruitment domaincontaining protein (CARD)8, a negative regulator of caspase-1 activity, have been associated with susceptibility to common inflammatory diseases, such as Crohns disease and rheumatoid arthritis. To investigate the role for genetic variants in the NLRP3 inflammasome in psoriasis susceptibility. In a patient sample comprising 1988 individuals from 491 families and 1002 healthy controls, genotypes for four selected single-nucleotide polymorphisms (SNPs) in NLRP3 (three SNPs) and CARD8 (one SNP) were determined by TaqMan (R) Allelic Discrimination. Using the transmission disequilibrium test (TDT), a significant increase in the transmission of the NLRP3 rs10733113G genotype to a subgroup of patients with more widespread psoriasis was demonstrated (P = 0.015). Using logistic regression analysis in 741 patients with psoriasis and 1002 controls, the CARD8 rs2043211 genotype was significantly different in cases and controls in overall terms [OR 1.3 (1.11.5), P = 0.004] and for both genders. Our data support the hypothesis that the inflammasome plays a role in psoriasis susceptibility.

Place, publisher, year, edition, pages
John Wiley and Sons, 2012
Keywords
CARD8, NLRP3, psoriasis
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-86644 (URN)10.1111/exd.12049 (DOI)000311406200009 ()
Note

Funding Agencies|Ingrid Asp Foundation||Welander Foundation||

Available from: 2012-12-20 Created: 2012-12-20 Last updated: 2017-12-06
Carlström, M., Ekman, A.-K., Petersson, S. & Enerbäck, C. (2012). Lack of Evidence for Association of VEGF Polymorphisms in Swedish Patients with Psoriasis [Letter to the editor]. Journal of Investigative Dermatology, 132(5), 1510-1513
Open this publication in new window or tab >>Lack of Evidence for Association of VEGF Polymorphisms in Swedish Patients with Psoriasis
2012 (English)In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 132, no 5, p. 1510-1513Article in journal, Letter (Other academic) Published
Abstract [en]

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Place, publisher, year, edition, pages
Nature Publishing Group, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-77087 (URN)10.1038/jid.2011.488 (DOI)000302856200032 ()
Available from: 2012-05-04 Created: 2012-05-04 Last updated: 2017-12-07
Shubbar, E., Vegfors, J., Carlström, M., Petersson, S. & Enerbäck, C. (2012). Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation. Breast Cancer Research and Treatment, 134(1), 71-80
Open this publication in new window or tab >>Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation
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2012 (English)In: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 134, no 1, p. 71-80Article in journal (Refereed) Published
Abstract [en]

Psoriasin (S100A7), originally identified in psoriasis, is a calcium-binding protein belonging to the multigenic S100 family. In high-grade ductal carcinoma in situ, psoriasin was identified as one of the most abundant transcripts. We have previously shown that psoriasin was induced by reactive oxygen species (ROS). Moreover, the downregulation of psoriasin by short hairpin RNA (shRNA) led to the reduced expression of vascular endothelial growth factor (VEGF) and inhibited tumor growth in vivo. The aim of the present study was to investigate whether psoriasin could have direct effects on endothelial cells. In this study we demonstrated that psoriasin increased VEGF expression in mammary epithelial cells. The treatment of endothelial cells with recombinant psoriasin increased proliferation comparable to that of recombinant VEGF protein. No change in proliferation was seen when endothelial cells were infected with psoriasin-expressing adenoviruses, suggesting that the proliferative effect of psoriasin was mediated by a specific receptor. Treatment with sRAGE, targeting the receptor for advanced glycation end products (RAGE), thus inhibited endothelial cell proliferation and tube formation enhanced by recombinant psoriasin. We showed that VEGF expression was not induced by hydrogen peroxide, when psoriasin was silenced by shRNA, which led to the hypothesis that psoriasin induces ROS. Indeed, psoriasin was shown to induce ROS in both endothelial and epithelial cells. Moreover, sRAGE inhibited the psoriasin-dependent generation of ROS in endothelial cells. Finally, treatment with antioxidant Bcl-2 protein abolished the effect of psoriasin on endothelial cell proliferation. Our data suggest that psoriasin expression in mammary epithelial cells leads to increased endothelial cell proliferation in a paracrine manner through RAGE. Psoriasin may therefore play a role in breast cancer progression by promoting oxidative stress response and angiogenesis.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-76132 (URN)10.1007/s10549-011-1920-5 (DOI)22189627 (PubMedID)000306437500008 (Scopus ID)
Note

funding agencies|Swedish Cancer Society||Swedish Psoriasis Association||Assar Gabrielsson Foundation||Welander Foundation||Tore Nilsson Foundation||

Available from: 2012-03-28 Created: 2012-03-28 Last updated: 2017-12-07
Vegfors, J., Petersson, S., Kovacs, A., Polyak, K. & Enerbäck, C. (2012). The Expression of Psoriasin (S100A7) and CD24 Is Linked and Related to the Differentiation of Mammary Epithelial Cells. PLoS ONE, 7(12)
Open this publication in new window or tab >>The Expression of Psoriasin (S100A7) and CD24 Is Linked and Related to the Differentiation of Mammary Epithelial Cells
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2012 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 7, no 12Article in journal (Refereed) Published
Abstract [en]

Psoriasin (S100A7), a member of the S100 family of calcium-binding proteins, is highly expressed in high-grade ductal carcinoma in situ (DCIS) and in the benign hyperproliferative skin disorder psoriasis. The gene that encodes psoriasin and many other S100 genes are located within a gene cluster on chromosome region 1q21, known as the epidermal differentiation complex. This cluster contains genes for several differentiation markers that play important roles in the terminal differentiation of the epidermis. The purpose of the present study was to evaluate the role of psoriasin in the differentiation process of mammary epithelial cells. Normal mammary epithelial cells (MCF10A) cultured in confluence and suspension, conditions known to induce psoriasin expression, demonstrated a shift towards a more differentiated phenotype indicated by an increase in the expression of the luminal differentiation markers CD24 and MUC1 and the reduced expression of the breast stem cell marker CD44. The expression of psoriasin and MUC1 was most pronounced in the CD24(+)-enriched fraction of confluent MCF10A cells. The shift towards a more differentiated phenotype was abolished upon the downregulation of psoriasin using short hairpin RNA (shRNA) and small interfering RNA (siRNA). Using specific inhibitors, we showed that psoriasin and CD24 expression was regulated by reactive oxygen species (ROS) and the nuclear factor (NF)-kappa B signaling pathways. While immunohistochemical analyses of DCIS showed heterogeneity, the expression of psoriasin and CD24 showed a similar staining pattern. Our findings suggest that the expression of psoriasin is linked to the luminal differentiation marker CD24 in mammary epithelial cells. Psoriasin demonstrated an essential role in the shift towards a more differentiated CD24(+) phenotype, supporting the hypothesis that psoriasin plays a role in the differentiation of luminal mammary epithelial cells.

Place, publisher, year, edition, pages
Public Library of Science, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-88366 (URN)10.1371/journal.pone.0053119 (DOI)000312829100122 ()
Note

Funding Agencies|Ingrid Asp Foundation||Swedish Cancer Society||Swedish Psoriasis Association||Welander Foundation||

Available from: 2013-02-04 Created: 2013-02-04 Last updated: 2017-12-06
Petersson, S., Shubbar, E., Yhr, M., Kovacs, A. & Enerbäck, C. (2011). Loss of ICAM-1 signaling induces psoriasin (S100A7) and MUC1 in mammary epithelial cells. Breast Cancer Research and Treatment, 125(1), 13-25
Open this publication in new window or tab >>Loss of ICAM-1 signaling induces psoriasin (S100A7) and MUC1 in mammary epithelial cells
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2011 (English)In: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 125, no 1, p. 13-25Article in journal (Refereed) Published
Abstract [en]

Psoriasin (S100A7), a member of the S100 gene family, is highly expressed in high-grade comedo ductal carcinoma in situ (DCIS), with a higher risk of local recurrence. Psoriasin is, therefore, a potential biomarker for DCIS with a poor prognosis. High-grade DCIS is characterized by a high proliferation rate and crowded cells, consequently, lose contact with the extracellular matrix. The aim of this study was, therefore, to elucidate the involvement of adhesion signals in the regulation of psoriasin. Protein expression was evaluated by Western blotting, flow cytometry, and immunohistochemistry, and using breast carcinoma SAGE databases available from the CGAP website. Intercellular adhesion molecule 1 (ICAM-1) was down-regulated in MCF10A cells using short hairpin RNA. We found a significant negative correlation between the expression of ICAM-1 and psoriasin, and a positive correlation between psoriasin and MUC1 in normal and DCIS SAGE libraries. In a cluster analysis of 34 adhesion molecules and 20 S100 proteins, we showed that SAGE libraries expressing the S100 proteins-psoriasin, calgranulin-A, and calgranulin-B-clustered together. Interestingly, the expression of all the three proteins correlated strongly to the oncogenic MUC1. We confirmed the negative correlation between ICAM-1 and psoriasin/MUC1, when normal and breast cancer cells were cultured in suspension and on collagen, respectively. The down-regulation of ICAM-1 by short hairpin RNA in MCF10A cells led to the induction of psoriasin, calgranulin-A, calgranulin-B, and MUC1, and we demonstrated that these up-regulations were not ROS dependent. By blocking the phospholipase C (PLC)-IP3 pathway in these cells, we showed that the induction of psoriasin diminished. The results suggest that psoriasin is an intracellular calcium-dependent target of the PLC pathway. Our findings suggest that the down-regulation of ICAM-1 in mammary epithelial cells may contribute both to the high expression of psoriasin seen in some high-grade DCIS tumors and to the induction of MUC1.

Place, publisher, year, edition, pages
Springer Science Business Media, 2011
Keywords
Breast cancer; Ductal carcinoma in situ; Psoriasin; Adhesion; ICAM-1; MUC1
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-63954 (URN)10.1007/s10549-010-0820-4 (DOI)000284956400002 ()
Note

The original publication is available at www.springerlink.com: Stina Petersson, E. Shubbar, M. Yhr, A. Kovacs and Charlotta Enerbäck, Loss of ICAM-1 signaling induces psoriasin (S100A7) and MUC1 in mammary epithelial cells, 2011, Breast Cancer Research and Treatment, (125), 1, 13-25. http://dx.doi.org/10.1007/s10549-010-0820-4 Copyright: Springer Science Business Media http://www.springerlink.com/

Available from: 2011-01-10 Created: 2011-01-10 Last updated: 2017-12-11
Anderson, K. S., Petersson, S., Wong, J., Lokko, N. N. & Enerbäck, C. (2010). Elevation of serum epidermal growth factor and interleukin 1 receptor antagonist in active psoriasis vulgaris. BRITISH JOURNAL OF DERMATOLOGY, 163(5), 1085-1089
Open this publication in new window or tab >>Elevation of serum epidermal growth factor and interleukin 1 receptor antagonist in active psoriasis vulgaris
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2010 (English)In: BRITISH JOURNAL OF DERMATOLOGY, ISSN 0007-0963, Vol. 163, no 5, p. 1085-1089Article in journal (Refereed) Published
Abstract [en]

Background Psoriatic plaques present a complex expression profile, including high levels of cytokines, chemokines and growth factors. Circulating cytokines have been suggested to reflect the activation status of the inflammatory process. Objectives To analyse 20 cytokines, chemokines and growth factors in 14 patients with psoriasis vulgaris at the start and during the course of ultraviolet B treatment. Methods A multiplex cytokine assay was used. Results We identified increased serum levels of epidermal growth factor (EGF) (mean 323 vs. 36 6 pg mL(-1), P = 0 0001), interleukin (IL)-1 receptor antagonist (mean 39 1 vs. 14 6 pg mL(-1), P = 0 02) and tumour necrosis factor-alpha (mean 7 5 vs. 4 5 pg mL(-1), P = 0 04) at baseline in patients with psoriasis compared with matched controls. None of these cytokines was correlated to the severity of the disease (Psoriasis Area and Severity Index) or decreased with phototherapy, suggesting that sources other than lesional skin contribute to the production of these cytokines. Using cluster analysis, we observed coordinate upregulation of EGF, IL-6, macrophage inflammatory protein-1 beta and vascular endothelial growth factor. Conclusions The sustained high expression of inflammatory circulating cytokines is a potential mechanism linking psoriasis with its extracutaneous comorbidities.

Place, publisher, year, edition, pages
Blackwell Publishing Ltd, 2010
Keywords
chemokines, cytokines, psoriasis
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-62157 (URN)10.1111/j.1365-2133.2010.09990.x (DOI)000283597500028 ()
Note

This is the authors’ version of the following article: K S Anderson, S Petersson, J Wong, N N Lokko and Charlotta Enerbäck, Elevation of serum epidermal growth factor and interleukin 1 receptor antagonist in active psoriasis vulgaris, 2010, BRITISH JOURNAL OF DERMATOLOGY, (163), 5, 1085-1089. which has been published in final form at: http://dx.doi.org/10.1111/j.1365-2133.2010.09990.x Copyright: Blackwell Publishing Ltd http://eu.wiley.com/WileyCDA/Brand/id-35.html

Available from: 2010-11-19 Created: 2010-11-19 Last updated: 2013-04-02
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