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Carlström, Maria
Publications (7 of 7) Show all publications
Ekman, A.-K., Sigurdardottir, G., Carlström, M., Kartul, N., Jenmalm, M. & Enerbäck, C. (2013). Systemically elevated Th1-, Th2- and Th17-associated chemokines in psoriasis vulgaris before and after ultraviolet B treatment. Acta Dermato-Venereologica, 93(5), 527-531
Open this publication in new window or tab >>Systemically elevated Th1-, Th2- and Th17-associated chemokines in psoriasis vulgaris before and after ultraviolet B treatment
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2013 (English)In: Acta Dermato-Venereologica, ISSN 0001-5555, E-ISSN 1651-2057, Vol. 93, no 5, p. 527-531Article in journal (Refereed) Published
Abstract [en]

Chemokines may contribute to the systemic inflammation that is linked to the increased risk of co-morbidities in patients with psoriasis. The aim of this study was to investigate circulating chemokines in patients with psoriasis and their relationship to disease severity. Analysis of plasma levels of chemokines in patients with psoriasis before narrowband ultraviolet B (UVB) therapy revealed increased expression of Th1-associated CXCL9 and -10, Th2-associated CCL17 and CCL22, and Th17-associated CCL20. CCL20 correlated with disease severity. UVB therapy reduced skin symptoms, but did not affect the chemokine levels in plasma. Anti-CD3 and anti-CD28-mediated activation of peripheral blood mononuclear cells (PBMCs) caused a higher secretion of Th2 cytokine interleukin (IL)-13 by PBMCs from patients with psoriasis than from healthy controls. The sustained high expression of inflammatory chemokines is a potential link to systemic inflammation in psoriasis. UVB therapy may be a more effective treatment of local rather than systemic inflammation.

Place, publisher, year, edition, pages
Society for Publication of Acta Dermato-Venereologica, 2013
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-102565 (URN)10.2340/00015555-1545 (DOI)000330327200006 ()23571825 (PubMedID)
Available from: 2013-12-13 Created: 2013-12-13 Last updated: 2018-10-12Bibliographically approved
Bivik, C., Carlström, M. & Enerbäck, C. (2012). Apoptosis has a role in the disturbed homeostasis of epidermal keratinocytes in psoriasis in JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol 132, issue , pp S79-S79. In: JOURNAL OF INVESTIGATIVE DERMATOLOGY (pp. S79-S79). Nature Publishing Group, 132
Open this publication in new window or tab >>Apoptosis has a role in the disturbed homeostasis of epidermal keratinocytes in psoriasis in JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol 132, issue , pp S79-S79
2012 (English)In: JOURNAL OF INVESTIGATIVE DERMATOLOGY, Nature Publishing Group , 2012, Vol. 132, p. S79-S79Conference paper, Published paper (Refereed)
Abstract [en]

n/a

Place, publisher, year, edition, pages
Nature Publishing Group, 2012
Series
JOURNAL OF INVESTIGATIVE DERMATOLOGY, ISSN 0022-202X
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-81502 (URN)000307814000441 ()
Available from: 2012-09-18 Created: 2012-09-18 Last updated: 2013-04-02
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]

n/a

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
Ekman, A.-K., Sigurdardottir, G., Carlström, M., Kartul, N., Jenmalm, M. & Enerbäck, C. (2012). Systemically elevated Th1-, Th2-and Th17-associated chemokines in psoriasis in JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol 132, issue , pp S28-S28. In: JOURNAL OF INVESTIGATIVE DERMATOLOGY (pp. S28-S28). Nature Publishing Group, 132
Open this publication in new window or tab >>Systemically elevated Th1-, Th2-and Th17-associated chemokines in psoriasis in JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol 132, issue , pp S28-S28
Show others...
2012 (English)In: JOURNAL OF INVESTIGATIVE DERMATOLOGY, Nature Publishing Group , 2012, Vol. 132, p. S28-S28Conference paper, Published paper (Refereed)
Abstract [en]

n/a

Place, publisher, year, edition, pages
Nature Publishing Group, 2012
Series
JOURNAL OF INVESTIGATIVE DERMATOLOGY, ISSN 0022-202X
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-81500 (URN)000307814000157 ()
Available from: 2012-09-18 Created: 2012-09-18 Last updated: 2013-04-02
Carlström, M., Ekman, A.-K., Söderkvist, P. & Enerbäck, C. (2011). Genetic support for a role for the inflammasome in psoriasis in BRITISH JOURNAL OF DERMATOLOGY, vol 165, issue 6, pp E2-E2. In: BRITISH JOURNAL OF DERMATOLOGY (pp. E2-E2). Wiley-Blackwell, 165(6)
Open this publication in new window or tab >>Genetic support for a role for the inflammasome in psoriasis in BRITISH JOURNAL OF DERMATOLOGY, vol 165, issue 6, pp E2-E2
2011 (English)In: BRITISH JOURNAL OF DERMATOLOGY, Wiley-Blackwell , 2011, Vol. 165, no 6, p. E2-E2Conference paper, Published paper (Refereed)
Abstract [en]

n/a

Place, publisher, year, edition, pages
Wiley-Blackwell, 2011
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-73327 (URN)000297320000005 ()
Available from: 2012-01-03 Created: 2012-01-02 Last updated: 2013-04-02
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