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Psoriasin (S100A7) promotes stress-induced angiogenesis.
Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology. (Ingrid Asp Psoriasis Research Center)
Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology. (Ingrid Asp Psoriasis Research Center)
University of Michigan, Ann Arbor, MI, U.S.A.
Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. (Ingrid Asp Psoriasis Research Center)
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2016 (English)In: British Journal of Dermatology, ISSN 0007-0963, E-ISSN 1365-2133, Vol. 175, no 6, 1263-1273 p.Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Vascular modifications occur early in the development of psoriasis, and angiogenesis is one of the key features in the pathogenesis of the disease.

OBJECTIVES: To identify the role of the S100 protein psoriasin in psoriasis-associated angiogenesis.

METHODS: The role of psoriasin in mediating angiogenesis was investigated by silencing psoriasin with small interfering RNA (siRNA) and measuring psoriasis-associated angiogenic factors in human epidermal keratinocytes. The secretion of psoriasin and the effect of psoriasin on general regulators of angiogenesis in keratinocytes, and on endothelial cell migration, proliferation, tube formation and production of angiogenic mediators, was evaluated.

RESULTS: Reactive oxygen species (ROS) and hypoxia induced the expression of psoriasin. Downregulation of psoriasin in keratinocytes using siRNA altered the ROS-induced expression of the psoriasis-associated angiogenic factors vascular endothelial growth factor (VEGF), heparin-binding epidermal growth factor-like growth factor, matrix metalloproteinase 1 and thrombospondin 1. Overexpression of psoriasin altered several regulators of angiogenesis and led to the secretion of psoriasin. Treatment with extracellular psoriasin induced proliferation, migration and tube formation in dermal-derived endothelial cells to a similar extent as VEGF and interleukin-17, and induced the expression and release of proangiogenic mediators. These effects were suggested to be mediated by the PI3K and nuclear factor kappa B pathways.

CONCLUSIONS: These findings suggest that psoriasin expression is promoted by oxidative stress in keratinocytes and amplifies the ROS-induced expression of angiogenic factors relevant to psoriasis. Moreover, extracellularly secreted psoriasin may act on dermal endothelial cells to contribute to key features angiogenesis.

Place, publisher, year, edition, pages
John Wiley & Sons, 2016. Vol. 175, no 6, 1263-1273 p.
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:liu:diva-133862DOI: 10.1111/bjd.14718ISI: 000391821300067PubMedID: 27155199OAI: oai:DiVA.org:liu-133862DiVA: diva2:1064663
Note

Funding agencies: Ingrid Asp Foundation; Welander Foundation; Swedish Psoriasis Association; Medical Research Council

Available from: 2017-01-12 Created: 2017-01-12 Last updated: 2017-02-15

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The full text will be freely available from 2017-10-05 18:34
Available from 2017-10-05 18:34

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Vegfors, JennyEkman, Anna-KarinBivik Eding, CeciliaEnerbäck, Charlotta
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Division of Neuro and Inflammation ScienceFaculty of Medicine and Health SciencesDepartment of Dermatology and Venerology
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CiteExportLink to record
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