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  • 1.
    Alexeyev, Oleg A
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Zouboulis, Christos C
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Shooting at skin propionibacterium acnes: to be or not to be on target2013Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 133, nr 9, s. 2292-2294Artikel i tidskrift (Refereegranskat)
  • 2.
    Brattsand, Maria
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Stefansson, Kristina
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Hubiche, Thomas
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Nilsson, Stefan K
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Fysiologisk kemi.
    Egelrud, Torbjörn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    SPINK9: a selective, skin-specific Kazal-type serine protease inhibitor.2009Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 129, nr 7, s. 1656-1665Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A previously unreported Kazal-type serine protease inhibitor, serine protease inhibitor Kazal type 9 (SPINK9), was identified in human skin. SPINK9 expression was strong in palmar epidermis, but not detectable or very low in non palmoplantar skin. Analysis of a human cDNA panel showed intermediate expression in thymus, pancreas, liver, and brain, and low or undetectable expression in other tissues. Using kallikrein-related peptidases (KLKs) 5, 7, 8, and 14, thrombin, trypsin, and chymotrypsin, inhibition with recombinant SPINK9 was seen only for KLK5 using low molecular weight substrates, with an apparent K(i) of 65 nM. Also KLK5 degradation of fibrinogen was totally inhibited by SPINK9. Slight inhibition of KLK8 using fibrinogen substrate could be observed using high concentrations of SPINK9. Analyses by surface plasmon resonance showed heterogeneous binding to SPINK9 of KLK5 and KLK8, but no binding of KLK7 or KLK14. KLK5 has been suggested to play a central role in skin desquamation as an initiating activating enzyme in proteolytic cascades formed by KLKs. An apparently KLK5-specific inhibitor, such as SPINK9, may play a significant regulatory role in such cascades. We suggest a possible role for SPINK9 in the site-specific epidermal differentiation of palms and soles.

  • 3.
    Brattsand, Maria
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Stefansson, Kristina
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Lundh, Christine
    Haasum, Ylva
    Egelrud, Torbjörn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    A proteolytic cascade of kallikreins in the stratum corneum2005Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 124, nr 1, s. 198-203Artikel i tidskrift (Refereegranskat)
  • 4.
    Bäckman, Assar
    et al.
    Astra Hässle AB, Umeå, Sweden.
    Strandén, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Brattsand, Maria
    Hansson, Lennart
    Astra Hässle AB, Umeå, Sweden.
    Egelrud, Torbjörn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Molecular cloning and tissue expression of the murine analog to human stratum corneum chymotryptic enzyme1999Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 113, nr 2, s. 152-5Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Human stratum corneum chymotryptic enzyme (SCCE) may play a central part in epidermal homeostasis. Its proposed function is to catalyze the degradation of intercellular structures, including desmosomes, in the stratum corneum as part of the desquamation process. In order to facilitate physiologic and pathophysiologic studies on SCCE we have looked for the corresponding murine enzyme. A cDNA obtained by reverse transcription-polymerase chain reaction with total RNA prepared from mouse tails as starting material was cloned, and the expression of the corresponding mRNA studied. The murine cDNA showed 77% homology to human SCCE cDNA. It had an open-reading frame encoding a protein comprising 249 amino acids with 82% amino acid sequence homology to human SCCE including the conserved sequences of the catalytic traid of mammalian serine proteases. The murine protein was deduced to have a 21 amino acid signal peptide and a four amino acid propeptide ending with a tryptic cleavage site, followed by a sequence motif identical to the N-terminal amino acid sequence of native active human SCCE. As in human SCCE the P2 position of the propeptide was occupied by an acidic amino acid residue, and the position corresponding to the suggested bottom of the primary substrate specificity pouch occupied by an asparagine residue. Analyses of mouse tissues by reverse transcriptase-polymerase chain reaction showed high expression in the skin, low expression in lung, kidney, brain, heart, and spleen, and no expression in liver or skeletal muscle. In situ hybridization of mouse skin showed expression in high suprabasal keratinocytes and in the luminal parts of hair follicles. Our results strongly suggest that we have cloned the murine analog of human SCCE cDNA.

  • 5. Carlén, Lina M
    et al.
    Sánchez, Fabio
    Bergman, Ann-Charlotte
    Becker, Susanne
    Hirschberg, Daniel
    Franzén, Bo
    Coffey, Jonathan
    Jörnvall, Hans
    Auer, Gert
    Alaiya, Ayodele A
    Ståhle, Mona
    Proteome analysis of skin distinguishes acute guttate from chronic plaque psoriasis.2005Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 124, nr 1Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Psoriasis is a disease with considerable heterogeneity in clinical presentation. This is the first study using two-dimensional gel electrophoresis to compare global protein expression patterns in lesional and non-lesional skin from subjects with acute guttate psoriasis associated with streptococcal throat infection and chronic plaque psoriasis. Samples from experimentally induced contact eczema and normal skin from healthy controls were also included. Proteins with statistically significant differences in expression were used in hierarchical cluster analyses resulting in separation of the different samples into groups. Chronic plaque and guttate psoriasis samples were distinctly separated, indicating that they represent discrete phenotypes at the protein expression level. Interestingly, there was a trend in which guttate psoriasis lesions clustered closer to eczema than to chronic plaque psoriasis lesions, indicating that the duration of the inflammatory reaction may affect clustering. Several of the differentially expressed proteins were identified by mass spectrometry.

  • 6. Caubet, Cécile
    et al.
    Jonca, Nathalie
    Brattsand, Maria
    Umeå universitet, Medicinsk fakultet, Folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Guerrin, Marina
    Bernard, Dominique
    Schmidt, Rainer
    Egelrud, Torbjörn
    Umeå universitet, Medicinsk fakultet, Folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Simon, Michel
    Serre, Guy
    Degradation of corneodesmosome proteins by two serine proteases of the kallikrein family, SCTE/KLK5/hK5 and SCCE/KLK7/hK7.2004Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 122, nr 5, s. 1235-1244Artikel i tidskrift (Refereegranskat)
  • 7. de Veer, Simon J.
    et al.
    Furio, Laetitia
    Swedberg, Joakim E.
    Munro, Christopher A.
    Brattsand, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Clements, Judith A.
    Hovnanian, Alain
    Harris, Jonathan M.
    Selective Substrates and Inhibitors for Kallikrein-Related Peptidase 7 (KLK7) Shed Light on KLK Proteolytic Activity in the Stratum Corneum2017Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 137, nr 2, s. 430-439Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Proteases have pivotal roles in the skin's outermost layer, the epidermis. In the stratum corneum, serine proteases from the kallikrein-related peptidase (KLK) family have been implicated in several key homeostatic processes, including desquamation. However, the precise contribution of specific KLKs to each process remains unclear. To address this, we used a chemical biology approach and designed selective substrates and inhibitors for KLK7, the most abundant KLK protease in the stratum corneum. The resulting KLK7 inhibitor is the most potent inhibitor of this protease reported to date (K-i = 140 pM), and displays at least 1,000-fold selectivity over several proteases that are related by function (KLK5 and KLK14) or specificity (chymotrypsin). We then used substrates and inhibitors for KLK5, KLK7, and KLK14 to explore the activity of each protease in the stratum corneum using casein zymography and an ex vivo desquamation assay. These experiments provide the most detailed assessment of each KLK's contribution to corneocyte shedding in the plantar stratum corneum, revealing that inhibition of KLK7 alone is sufficient to block shedding, whereas KLK5 is also a major contributor. Collectively, these findings unveil chemical tools for studying KLK activity and demonstrate their potential for characterizing KLK biological functions in epidermal homeostasis.

  • 8.
    Ekholm, I Elisabeth
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Brattsand, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Egelrud, Torbjörn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Stratum corneum tryptic enzyme in normal epidermis: a missing link in the desquamation process?2000Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 114, nr 1, s. 56-63Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Stratum corneum chymotryptic enzyme may be important in desquamation. It has also been suggested that other proteases, especially stratum corneum tryptic enzyme, may be involved. Stratum corneum tryptic enzyme has been purified and its cDNA has been cloned. Results from expression analyses indicate that stratum corneum tryptic enzyme is as skin specific as stratum corneum chymotryptic enzyme. In this work we have produced and characterized antibodies specific for stratum corneum tryptic enzyme. We have also by means of biochemical, immunochemical, and immunohistochemical methods performed studies on stratum corneum tryptic enzyme in normal human epidermis. Antibodies against bacterial recombinant stratum corneum tryptic enzyme were produced and purified by affinity chromatography. Two types of antibodies were obtained: one reacting only with pro-stratum corneum tryptic enzyme and one specific for the catalytically active part of stratum corneum tryptic enzyme. Immunohistochemistry with the antibodies reacting with pro-stratum corneum tryptic enzyme showed a staining pattern similar to stratum corneum chymotryptic enzyme-specific antibodies, i.e., the expression was confined to cornifying epithelia with a need of desquamation-like processes. Extracts of tape strips with superficial human stratum corneum were found to contain precursors as well as active forms of stratum corneum tryptic enzyme and stratum corneum chymotryptic enzyme. The enzymes had maximal activity at pH 8, but both had considerable activity also at pH 5.5. The results were compatible for a role of stratum corneum tryptic enzyme in desquamation. Stratum corneum tryptic enzyme may act in concert with stratum corneum chymotryptic enzyme and/or function as a stratum corneum chymotryptic enzyme-activating enzyme. The presence in normal superficial stratum corneum of precursors as well as of active forms of stratum corneum chymotryptic enzyme and stratum corneum tryptic enzyme, and the activity of both enzymes over a broad range of pH-values, suggest some possible ways by which the desquamation may be regulated.

  • 9. Fredholm, Simon
    et al.
    Willerslev-Olsen, Andreas
    Met, Özcan
    Kubat, Linda
    Gluud, Maria
    Mathiasen, Sarah L.
    Friese, Christina
    Blümel, Edda
    Petersen, David L.
    Hu, Tengpeng
    Nastasi, Claudia
    Lindahl, Lise M.
    Buus, Terkild B.
    Krejsgaard, Thorbjørn
    Wasik, Mariusz A.
    Kopp, Katharina L.
    Koralov, Sergei B.
    Persson, Jenny L.
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Division of Experimental Cancer Research, Department of Translational Medicine, Lund University, Clinical Research Centre, Malmö, Sweden.
    Bonefeld, Charlotte M.
    Geisler, Carsten
    Woetmann, Anders
    Iversen, Lars
    Becker, Jürgen C.
    Odum, Niels
    SATB1 in Malignant T Cells2018Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 138, nr 8, s. 1805-1815Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Deficient expression of SATB1 hampers thymocyte development and results in inept T-cell lineages. Recent data implicate dysregulated SATB1 expression in the pathogenesis of mycosis fungoides, the most frequent variant of cutaneous T-cell lymphoma. Here, we report on a disease stage-associated decrease of SATB1 expression and an inverse expression of STAT5 and SATB1 in situ. STAT5 inhibited SATB1 expression through induction of microRNA-155. Decreased SATB1 expression triggered enhanced expression of IL-5 and IL-9 (but not IL-6 and IL-32), whereas increased SATB1 expression had the opposite effect, indicating that the microRNA-155 target SATB1 is a repressor of IL-5 and IL-9 in malignant T cells. In accordance, inhibition of STAT5 and its upstream activator JAK3 triggered increased SATB1 expression and a concomitant suppression of IL-5 and IL-9 expression in malignant T cells. In conclusion, we provide a mechanistic link between the proto-oncogenic JAK3/STAT5/microRNA-155 pathway, SATB1, and cytokines linked to CTCL severity and progression, indicating that SATB1 dysregulation is involved in cutaneous T-cell lymphoma pathogenesis.

  • 10.
    Gu, Xiaolian
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Lundqvist, Elisabet N
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Coates, Philip J
    Thurfjell, Niklas
    Wettersand, Emma
    Nylander, Karin
    Dysregulation of TAp63 mRNA and protein levels in psoriasis2006Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 126, nr 1, s. 137-141Artikel i tidskrift (Refereegranskat)
  • 11.
    Gu, Xiaolian
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Nylander, Elisabet
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Coates, Philip J.
    Fahraeus, Robin
    Nylander, Karin
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Correlation between Reversal of DNA Methylation and Clinical Symptoms in Psoriatic Epidermis Following Narrow-Band UVB Phototherapy2015Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 135, nr 8, s. 2077-2083Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Epigenetic modifications by DNA methylation are associated with a wide range of diseases. Previous studies. in psoriasis have concentrated on epigenetic changes in immune cells or in total skin biopsies that include stromal-associated changes. In order to improve our understanding of the role of DNA methylation in psoriasis, we sought to obtain a comprehensive DNA methylation signature specific for the epidermal component of psoriasis and to analyze methylation changes during therapy. Genome-wide DNA methylation profiling of epidermal cells from 12 patients undergoing narrow-band UVB phototherapy and 12 corresponding healthy controls revealed a distinct DNA methylation pattern in psoriasis compared with controls. A total of 3,665 methylation variable positions (MVPs) were identified with an overall hypomethylation in psoriasis patient samples. DNA methylation pattern was reversed at the end of phototherapy in patients showing excellent clinical improvement. Only 7% of phototherapy-affected MVPs (150 out of 2,108) correlate with nearby gene expression. Enrichment of MVPs in enhancers indicates tissue-specific modulation of the transcriptional regulatory machinery in psoriasis. Our study identified key epigenetic events associated with psoriasis pathogenesis and helps understand the dynamic DNA methylation landscape in the human genome.

  • 12. Hachem, Jean-Pierre
    et al.
    Wagberg, Fredrik
    Schmuth, Matthias
    Crumrine, Debra
    Lissens, Willy
    Jayakumar, Arumugam
    Houben, Evi
    Mauro, Theodora M
    Leonardsson, Göran
    Brattsand, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Egelrud, Torbjorn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Roseeuw, Diane
    Clayman, Gary L
    Feingold, Kenneth R
    Williams, Mary L
    Elias, Peter M
    Serine protease activity and residual LEKTI expression determine phenotype in Netherton syndrome2006Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 126, nr 7, s. 1609-21Artikel i tidskrift (Refereegranskat)
  • 13. Jacob, N
    et al.
    Rüschendorf, F
    Schmitt-Egenolf, Marcus
    Department of Dermatology, Humboldt University, Charité, Berlin, Germany.
    Hennies, HC
    Friedl, G
    Ständer, M
    Wienker, TF
    Reis, A
    Traupe, H
    Promoter polymorphism at -238 of the tumor necrosis factor alpha gene is not associated with early onset psoriasis when tested by the transmission disequilibrium test1999Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 112, nr 4, s. 513-514Artikel i tidskrift (Refereegranskat)
  • 14.
    Karlsson, Terese
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Mark, Elisabeth B
    Henriksson, Roger
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hedman, Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Redistribution of LRIG proteins in psoriasis2008Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 128, nr 5, s. 1192-1195Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The human leucine-rich repeats and immunoglobulin-like domains (LRIG) family is composed of three members, LRIG1, -2, and -3, which are all expressed in human skin. LRIG1 negatively regulates growth factor signaling and is involved in the regulation of epidermal stem cell quiescence. Ablation of Lrig1 in mice results in psoriasiform epidermal hyperplasia. Hence, the LRIG proteins may be important for epidermal homeostasis and in psoriasis. Therefore, we analyzed the LRIG mRNA levels and the cellular and subcellular distribution of LRIG proteins in normal and psoriatic skin. The mRNA levels of LRIG1, -2, and -3 were not significantly different in psoriatic epidermis compared to clinically normal epidermis from the same patient. Immunohistochemistry showed that all three LRIG proteins were expressed in unique and specific patterns both in normal and psoriatic skin. Intriguingly, in psoriatic epidermis, the LRIG protein expression patterns were altered compared to normal skin. These results indicate that the LRIG proteins may have a role in epidermal homeostasis and psoriasis.

  • 15. Lindqvist, Ulla
    et al.
    Theander, Elke
    Husmark, Tomas
    Larsson, Per
    Teleman, Annika
    Alenius, Gerd-Marie
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Reumatologi.
    Geijer, Mats
    The Swedish Early Psoriatic Arthritis (SWEPSA) registry 5-year follow-up: Slow radiographic progression with highest scores in male feet and patients with baseline x-ray abnormalities2015Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 135, nr Suppl. 3, s. S1-S1Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    The aim is to describe early X-ray findings in psoriatic arthritis (PsA) from the SwePsA registry using the Wassenberg score, evaluate progression of structural damage, analyze correlations to clinical disease parameters and identify predictors of progressive radiographic joint disease.

  • 16. Meding, Birgitta
    et al.
    Järvholm, Bengt
    Umeå universitet, Medicinsk fakultet, Folkhälsa och klinisk medicin, Yrkes- och miljömedicin.
    Incidence of hand eczema-a population-based retrospective study.2004Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 122, nr 4, s. 873-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    When etiological relationship is of interest, the incidence rate is a preferred measure. The aim of the present retrospective study was to estimate the incidence rate of self-reported hand eczema in a sample from the general population and to study the relation of this to age, sex, and atopy. A questionnaire was mailed to 3000 individuals aged 20-65 y, randomly selected from the population register of Göteborg, Sweden. This gave a response rate of 73.9%. Questions were asked about ever having had hand eczema, time of onset of the disease, history of childhood eczema, and history of asthma/hay fever. The crude incidence rate of self-reported hand eczema was 5.5 cases per 1000 person-years (females 7.1 and males 4.0). There was no difference, however, in incidence rate between women and men above 30 y of age. In a Poisson regression analysis, female sex, childhood eczema, and asthma/hay fever were all significantly associated with hand eczema, but only at ages below 30 y. A moderate influence of recall bias and a probable tendency to underreport imply that the incidence rates presented are to be considered as minimum rates.

  • 17. Murakami, M.
    et al.
    Kaneko, T.
    Kishibe, M.
    Brattsand, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Morhenn, V.
    Ishida-Yamamoto, A.
    Iizuka, H.
    Shirakata, Y.
    Sayama, K.
    Multiple over-expression of kallikrein related peptidases contributes to the inflammatory hyperkeratotic change with abnormal desquamation in lesions of palmoplantar pustulosis2012Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 132, s. S62-S62Artikel i tidskrift (Övrigt vetenskapligt)
  • 18.
    Pasonen-Seppänen, Sanna
    et al.
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    Karvinen, Susanna
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    Törrönen, Kari
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    Hyttinen, Juha
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    Jokela, Tiina
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    Lammi, Mikko
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    Tammi, Markku
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    Tammi, Raija
    Department of Anatomy, University of Kuopio, Kuopio, Finland.
    EGF upregulates, whereas TGF-beta downregulates, the hyaluronan synthases Has2 and Has3 in organotypic keratinocyte cultures: correlations with epidermal proliferation and differentiation.2003Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 120, nr 6, s. 1038-1044, artikel-id 12787132Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Hyaluronan, a major extracellular matrix molecule in the vital cell layers of skin epidermis, has been suggested to support proliferation and migration of keratinocytes, during challenges like wounding and inflammation. An organotypic keratinocyte culture originated from continuous rat epidermal keratinocyte cell line was subjected to the proliferative and antiproliferative growth factors epidermal growth factor and transforming growth factor beta, respectively, to study their influence on hyaluronan synthesis and epidermal morphology. Epidermal growth factor induced a 4-fold increase of epidermal hyaluronan concentration. This was associated with upregulation of the hyaluronan synthases Has2 and Has3, and the hyaluronan receptor CD44. 5-Bromo-2'-deoxyuridine labeling, basal cell height, and the thickness of vital epidermis were increased, reflecting the hyperplastic effects of epidermal growth factor. The expression of keratin 10 and the maturation of filaggrin were inhibited, and epidermal permeability barrier became less efficient, indicating compromised terminal differentiation by epidermal growth factor. In contrast, transforming growth factor beta reduced the content of hyaluronan and the mRNA of Has2 and Has3. At the same time, transforming growth factor beta suppressed keratinocyte proliferation and epidermal thickness, but retained intact differentiation. The results suggest that epidermal hyaluronan synthesis, controlled by epidermal growth factor and transforming growth factor beta through changes in the expression of Has2 and Has3, correlates with epidermal proliferation, thickness, and differentiation.

  • 19.
    Schmitt-Egenolf, Marcus
    et al.
    Department of Dermatology, University of Kiel, Germany.
    Boehncke, WH
    Christophers, E
    Ständer, M
    Sterry, W
    Type I and type II psoriasis show a similar usage of T-cell receptor variable regions1991Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 97, nr 6, s. 1053-1056Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In nonpustular psoriasis, principally two forms can be distinguished [Christophers E. Henseler T: Patient subgroups and the inflammatory pattern in psoriasis. Acta Dermatol Venereol 69(suppl 151):88-92, 1989): Type I frequently shows positive family history, linkage disequilibrium for human leucocyte antigens (HLAs) Cw6, B13 and Bw57 as well as an early onset. Type II manifests itself around the 5th decade, it is more frequently than normal associated with Cw2 and B27. In the light of this association with HLAs an autoimmune pathogenesis has been discussed. In order to investigate the pathogenetic function of T cells we obtained biopsies from patients with type I (n = 10) and type II (n = 10) psoriasis. Three-step peroxidase staining was performed using a panel of monoclonal antibodies directed against five variable (V) regions of the beta chain (V beta 5a, V beta 5b, V beta 6, V beta 8, V beta 12) and one of the alpha chain (V alpha 2) of the T cell receptor (TCR). Positive or negative selection of a particular TCR V region could not be detected in the demonstrable repertoire. Furthermore, the usage of the V regions under investigation revealed a similar pattern in the two forms of psoriasis.

  • 20.
    Schmitt-Egenolf, Marcus
    et al.
    Department of Dermatology, University of Ulm, Ulm, Germany.
    Boehncke, WH
    Ständer, M
    Eiermann, TH
    Sterry, W
    Oligonucleotide typing reveals association of type I psoriasis with the HLA-DRB1*0701/2, -DQA1*0201, -DQB1*0303 extended haplotype1993Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 100, nr 6, s. 749-752Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Although the pathogenesis of psoriasis is still a matter of debate, there are several lines of evidence supporting the concept of this disease being immunologically mediated with T cells playing a crucial role. Because a considerable portion of the cellular infiltrate in psoriasis consists of activated T-helper cells, expression of HLA class II antigens might be of particular importance for the understanding of its pathogenesis. Therefore, we investigated the HLA type of patients with type I (early onset, positive family history) and type II (late onset, no family history) psoriasis by means of serology (n = 89) and genotyping using sequence-specific oligonucleotide probes (n = 64). Serologic analysis of class I documented the association of type I psoriasis with HLA-Cw6, -B13, and -B57, whereas type II psoriasis showed a weaker correlation with HLA-Cw2 and -B27. Genotyping using SSO for class II detected the elevation of the HLA-DRB1*0701/2 allele frequency from 13% in normal population to 36% in type I, but only to 15% in type II psoriatics. Moreover, positive correlations with type I psoriasis were detected for HLA-DQA1*0201 and HLA-DQB1*0303. The HLA-DRB1*0701/2, -DQA1*0201, -DQB1*0303 extended haplotype was found exclusively in type I psoriasis. This is the first report documenting the association of distinct HLA class II alleles with type I psoriasis as detected on the DNA level, an approach both more specific and more sensitive when compared to serology.

  • 21.
    Schmitt-Egenolf, Marcus
    et al.
    Department of Dermatology, School of Medicine (Charité), Humboldt University, Berlin, Germany & Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, University of Vienna Medical School, Vienna, Austria.
    Eiermann, TH
    Boehncke, WH
    Ständer, M
    Sterry, W
    Familial juvenile onset psoriasis is associated with the human leukocyte antigen (HLA) class I side of the extended haplotype Cw6-B57-DRB1*0701-DQA1*0201-DQB1*0303: a population- and family-based study1996Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 106, nr 4, s. 711-714Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    To further evaluate the nature of the HLA association with psoriasis, HLA haplotypes of 60 patients with type 1 (early onset, positive family history) and 30 patients with type II (late onset, no family history) psoriasis were investigated by polymerase chain reaction sequence-specific oligonucleotide hybridization (HLA class II) and serology (HLA class I). Ethnically matched blood donors (146) served as controls. In type I, but not type II psoriasis, the Caucasian HLA extended haplotype (EH) Cw6-B57-DRB1*0701-DQA1*0201-DQB1*0303 named according to the B allele EH-57.1 was highly significantly overrepresented (p cor= 0.00021). This particular EH was present in 35% of type I psoriatics but only 2% of controls. EH-57.1+ individuals therefore carry a 26 times higher risk of developing type I psoriasis than individuals who are EH-57.1-negative Further analysis of individual HLA alleles revealed that within EH-57.1, HLA class I antigens (Cw6-B57) were associated to a much higher extent with type I psoriasis than the HLA class II alleles (DRB1*0701-DQA1*0201-DQB1* 0303). Pedigree analysis of three multiply affected families over three generations revealed a cosegregation of disease with EH-57.1. These results strongly suggest that a gene for familial psoriasis is associated with the class I side of the extended haplotype Cw6-B57-DRB1*0701-DQA1*0201-DQB1*0303.

  • 22.
    Sjödin, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Guo, Dongsheng
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hofer, Per-Åke
    Henriksson, Roger
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hedman, Håkan
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Mammaglobin in normal human sweat glands and human sweat gland tumors2003Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 121, nr 2, s. 428-429Artikel i tidskrift (Övrigt vetenskapligt)
  • 23.
    Stefansson, Kristina
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Brattsand, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Roosterman, Dirk
    Kempkes, Cordula
    Bocheva, Georgeta
    Steinhoff, Martin
    Egelrud, Torbjörn
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Dermatologi och venereologi.
    Activation of proteinase-activated receptor-2 by human kallikrein-related peptidases2008Ingår i: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 128, nr 1, s. 18-25Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Proteinase-activated receptor-2 (PAR2) is a seven transmembrane spanning, G-protein-coupled receptor, present on the membrane of many cell types including keratinocytes. In skin, PAR2 is suggested to play a regulatory role during inflammation, epidermal barrier function, and pruritus. PAR2 is activated by trypsin-like proteases by a unique mechanism where cleavage of the receptor leads to the release of a small peptide, which activates the receptor as a tethered ligand. The endogenous activators of PAR2 on keratinocytes have not been identified as of yet. Potential candidates are kallikrein-related peptidases (KLKs) expressed by epidermal cells. Therefore, the ability of four human skin-derived KLKs was examined with regard to their capacity to activate PAR2 in vitro. PAR2 cleavage was followed by immunofluorescence analysis and functional activation by measurements of changes in intracellular calcium levels. We found that KLK5 and KLK14, but neither KLK7 nor KLK8, induced PAR2 signalling. We conclude that certain, but not all, epidermal KLKs are capable of activating PAR2. We could also show the coexpression of KLK14 and PAR2 receptor in inflammatory skin disorders. These in vitro results suggest that KLKs may take part in PAR2 activation in the epidermis and thereby in PAR2-mediated inflammatory responses, including epidermal barrier repair and pruritus. The role of KLKs in PAR2 activation in vivo remains to be elucidated.

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