Molecular Cloning, Occurrence, and Expression of a Novel Partially Secreted Protein “Psoriasin” That Is Highly Up-Regulated in Psoriatic Skin

Madsen, Peder; Rasmussen, Hanne H.; Leffers, Henrik; Honoré, Bent; Dejgaard, Kurt; Olsen, Eydfinnur; Kiil, J; Walbum, Else; Andersen, Anders H.; Basse, Bodil; Lauridsen, Jette B.; Ratz, Gitte P.; Celis, Ariana; Vandekerckhove, Joël; Celis, Julio E.

doi:10.1111/1523-1747.ep12484041

Cited by 381 publications

(371 citation statements)

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“…For example, in addition to their association with disease severity in RA, 4 S100/calgranulins have been linked to disease progression in inflammatory bowel disease. 36,37 Furthermore, strongly increased expression of a member of this family of molecules, psoriasin, has been demonstrated in psoriatic lesions compared with adjacent unaffected skin in human subjects, 38 thus further supporting the premise that S100/calgranulins may not simply be 'innocent bystanders', but, rather, by virtue of their engagement of RAGE, 1 active participants in the host inflammatory response. We speculate that triggered by interaction with accumulating S100/calgranulins, activation of RAGE engages key signalling pathways linked to proinflammatory responses, such as MAP kinases and NF-B, thereby amplifying expression of molecules linked to chronic cellular perturbation and tissue destruction.…”

Section: Rage 82s Allele and Association With Rheumatoid Arthritismentioning

confidence: 71%

RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response

et al. 2002

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Section: Rage 82s Allele and Association With Rheumatoid Arthritismentioning

confidence: 71%

RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response

et al. 2002

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“…1) . We also analyzed fractions that did not induce IFNs in pDCs, namely fractions 21 and 25, which contained 5999 Da peptide elafin [26], and the 11 366 Da protein psoriasin (S100A7) [18,19], respectively ( Fig. 1).…”

Section: Resultsmentioning

confidence: 99%

Cationic antimicrobial peptides in psoriatic skin cooperate to break innate tolerance to self‐DNA

et al. 2014

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Psoriasis is a T-cell-mediated skin autoimmune disease characterized by the aberrant activation of dermal dendritic cells (DCs) and the sustained epidermal expression of antimicrobial peptides. We have previously identified a link between these two events by showing that the cathelicidin antimicrobial peptide LL37 has the ability to trigger selfnucleic acid mediated activation of plasmacytoid DCs (pDCs) in psoriatic skin. Whether other cationic antimicrobial peptides exert similar activities is unknown. By analyzing heparin-binding HPLC fractions of psoriatic scales, we found that human beta-defensin (hBD)2, hBD3, and lysozyme are additional triggers of pDC activation in psoriatic skin lesions. Like LL37, hBD2, hBD3, and lysozyme are able to condense self-DNA into particles that are endocytosed by pDCs, leading to activation of TLR9. In contrast, other antimicrobial peptides expressed in psoriatic skin including elafin, hBD1, and psoriasin (S100A7) did not show similar activities. hBD2, hBD3, and lysozyme were detected in psoriatic skin lesions in the vicinity of pDCs and found to cooperate with LL37 to induce high levels of IFN production by pDCs, suggesting their concerted role in the pathogenesis of psoriasis.Keywords: Antimicrobial peptides r Plasmacytoid DC r Psoriasis r Skin r Toll-like receptor Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionPsoriasis is a common T-cell-mediated inflammatory disease of the skin, which, in its most prevalent form, is characterized by the appearance of scaly erythematous plaques that may cover large Correspondence: Dr. Michel Gilliet e-mail: Michel.gilliet@chuv.ch areas of the patient's body [1][2][3]. A key feature of psoriasis is the abnormal activation of dendritic cell (DC) subsets in the dermal compartment leading to the downstream T-cell-mediated autoimmune cascade [4]. A role for plasmacytoid DCs (pDCs) producing type I IFNs appears to be central in this process. pDC-derived * These authors contributed equally to this work.www.eji-journal.eu 204Roberto Lande et al. Eur. J. Immunol. 2015. 45: 203-213 IFNs activate conventional DCs that stimulate autoimmune T cells to migrate into the epidermis [5]. Here, these T cells produce Th17 cytokines 7], which directly initiate keratinocyte proliferation and an abnormal epidermal differentiation pattern [8,9]. Another key feature of psoriasis is the excessive production of antimicrobial peptides (AMPs) and proteins by keratinocytes [10][11][12]. These AMPs are best known for their role in killing pathogenic microorganisms such as Gram-positive and Gramnegative bacteria, protozoa, fungi, as well as some viruses [13]. The antimicrobial activity of AMPs has been ascribed to their unique cationic and amphiphatic structure, which allows interaction with and disruption of microbial membranes containing a high degree of negative charges. Three major antimicrobial peptide classes found in psoriatic skin are the cathelicidin, β-defensins, or S100 proteins. ...

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“…We and others have demonstrated that psoriasin may be secreted by but also located in the cytoplasm and the nucleus of the cells expressing it [9,30]. To examine possible differences in extracellular and intracellular effects of psoriasin on endothelial cell proliferation, we treated endothelial cells with recombinant psoriasin protein and infected endothelial cells with psoriasin-expressing adenovirus.…”

Section: Discussionmentioning

confidence: 99%

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Shubbar

Vegfors

Carlström

et al. 2011

Breast Cancer Res Treat

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Psoriasin (S100A7), originally identified in psoriasis, is a calcium-binding protein belonging to the multigenic S100 family. In high-grade ductal carcinoma in situ (DCIS), 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 VEGF and inhibited tumour 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.

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Molecular Cloning, Occurrence, and Expression of a Novel Partially Secreted Protein “Psoriasin” That Is Highly Up-Regulated in Psoriatic Skin

Cited by 381 publications

References 54 publications

RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response

RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response

Cationic antimicrobial peptides in psoriatic skin cooperate to break innate tolerance to self‐DNA

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

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