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Special Issue "Molecular Mechanisms and Pathology of Psoriasis"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2019).

Special Issue Editors

Dr. Roxane Pouliot
Website
Guest Editor
Université Laval, Québec, QC, Canada
Interests: skin, psoriasis, tissue engineering
Dr. Sylvain Guérin

Guest Editor
Université Laval, Québec, QC, Canada
Interests: tissue reconstruction, uveal melanoma, tissue-engineered human cornea

Special Issue Information

Dear Colleagues,

Psoriasis is a serious skin disorder affecting men, women and children without any racial distinction. This pathology is characterized by the presence of red or pink patches covered by thick gray danders. Currently, the exact cause of this skin disorder is not known. However, certain mechanisms such as hyperproliferation of keratinocytes, abnormal differentiation of keratinocytes and infiltration of the skin by inflammatory cells have a role to play in the onset of this disease. Several models have been presented in recent years, including both animal and in vitro human models. However, none of these show a complete phenotype of psoriasis. In the field of science, genetically modified mouse models or xenotransplantations allow to see certain characteristics of psoriasis which makes it possible to study different aspects of the pathology. In addition, certain in vitro models made from human cells are more and more similar to the pathology and therefore make it possible to study different aspects of this disease. This Special Issue of IJMS provides a comprehensive overview of the most advanced in vivo and in vitro models that feature reliable characteristics of psoriasis.

Dr. Roxane Pouliot
Dr. Sylvain Guérin
Guest Editors

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Published Papers (9 papers)

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Open AccessArticle
Dihydrochalcone Derivatives from Populus balsamifera L. Buds for the Treatment of Psoriasis
Int. J. Mol. Sci. 2020, 21(1), 256; https://doi.org/10.3390/ijms21010256 - 30 Dec 2019
Cited by 2
Abstract
Psoriasis is a skin disorder characterized by epidermal hyperplasia, hyperkeratosis, and inflammation. The treatments currently available on the market only improve patients’ quality of life and are associated with undesirable side effects. Thus, research leading to the development of new, effective, and safer [...] Read more.
Psoriasis is a skin disorder characterized by epidermal hyperplasia, hyperkeratosis, and inflammation. The treatments currently available on the market only improve patients’ quality of life and are associated with undesirable side effects. Thus, research leading to the development of new, effective, and safer therapeutic agents is still relevant. Populus balsamifera L. buds were used traditionally by Native Americans to treat various skin pathologies such as eczema and psoriasis. In this study, the antipsoriatic activities of dihydrochalcone derivatives from Populus balsamifera L. buds, known as balsacones, were investigated. The experiments were performed in vitro using a psoriatic skin substitute model. Also, anti-inflammatory and antioxidant activities were investigated. The tested balsacones showed promising antipsoriatic properties by slowing down cell growth and by regulating the expression of involucrin, loricrin, and Ki67 better than methotrexate in psoriatic substitutes. All five tested compounds could be an effective topical treatment for psoriasis, with promising anti-inflammatory and antioxidant actions that may contribute to clinical improvement in patients with psoriasis. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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Open AccessArticle
Lysosome Alterations in the Human Epithelial Cell Line HaCaT and Skin Specimens: Relevance to Psoriasis
Int. J. Mol. Sci. 2019, 20(9), 2255; https://doi.org/10.3390/ijms20092255 - 07 May 2019
Cited by 2Correction
Abstract
Despite the constantly updated knowledge regarding the alterations occurring in the cells of patients with psoriasis, the status and the role of the lysosome, a control center of cell metabolism, remain to be elucidated. The architecture of the epidermis is largely regulated by [...] Read more.
Despite the constantly updated knowledge regarding the alterations occurring in the cells of patients with psoriasis, the status and the role of the lysosome, a control center of cell metabolism, remain to be elucidated. The architecture of the epidermis is largely regulated by the action of lysosomes, possibly activating signaling pathways in the cellular crosstalk of keratinocytes—epidermal cells—with infiltrating immune cells. Thus, in the present study, lysosome alterations were examined in vitro and in situ using a two-dimensional (2D) keratinocyte model of HaCaT cells with “psoriasis-like” inflammation and skin specimens, respectively. Specific fluorescence and immunohistochemical staining showed an augmented level of acidic organelles in response to keratinocyte activation (mimicking a psoriatic condition while maintaining the membrane integrity of these structures) as compared with the control, similar to that seen in skin samples taken from patients. Interestingly, patients with the most pronounced PASI (Psoriasis Area and Severity Index), BSA (Body Surface Area), and DLQI (Dermatology Life Quality Index) scores suffered a high incidence of positive lysosomal-associated membrane protein 1 (LAMP1) expression. Moreover, it was found that the gene deregulation pattern was comparable in lesioned (PP) and non-lesioned (PN) patient-derived skin tissue, which may indicate that these alterations occur prior to the onset of the characteristic phenotype of the disease. Changes in the activity of genes encoding the microphthalmia family (MiT family) of transcription factors and mammalian target of rapamycin complex 1 (MTORC1) were also observed in the in vitro psoriasis model, indicating that the biogenesis pathway of this arm is inhibited. Interestingly, in contrast to the keratinocytes of HaCaT with “psoriasis-like” inflammation, LAMP1 was up-regulated in both PP and PN skin, which can be a potential sign of an alternative mechanism of lysosome formation. Defining the molecular profile of psoriasis in the context of “the awesome lysosome” is not only interesting, but also desired; therefore, it is believed that this paper will serve to encourage other researchers to conduct further studies on this subject. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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Open AccessArticle
Infiltration of T Cells into a Three-Dimensional Psoriatic Skin Model Mimics Pathological Key Features
Int. J. Mol. Sci. 2019, 20(7), 1670; https://doi.org/10.3390/ijms20071670 - 03 Apr 2019
Cited by 4
Abstract
Psoriasis is an autoimmune chronic dermatosis that is T cell-mediated, characterized by epidermal thickening, aberrant epidermal differentiation and inflammatory infiltrates, with a dominant Th1 and Th17 profile. Additional in vitro models are required to study the complex interactions between activated T cells and [...] Read more.
Psoriasis is an autoimmune chronic dermatosis that is T cell-mediated, characterized by epidermal thickening, aberrant epidermal differentiation and inflammatory infiltrates, with a dominant Th1 and Th17 profile. Additional in vitro models are required to study the complex interactions between activated T cells and skin cells, and to develop new, more effective treatments. We have therefore sought to model this psoriatic inflammation by the generation of tissue-engineered immunocompetent tissues, and we have investigated the response of activated T-cell infiltration in models produced with lesional psoriatic skin cells on major hallmarks of psoriasis. The immunocompetent lesional skin model displayed a delayed onset of epidermal differentiation, an hyperproliferation of the basal keratinocytes, a drastic increase in the secretion of proinflammatory cytokines, and a disturbed expression of key transcription factors, as observed in lesional plaques, suggesting a crucial importance of combining the pathological phenotype of cutaneous cells to T cells in order to generate a relevant model for psoriasis. Finally, we found this skin model to be responsive to methotrexate treatment, making it a valuable tool for drug development. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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Open AccessArticle
The Tissue-Engineered Human Psoriatic Skin Substitute: A Valuable In Vitro Model to Identify Genes with Altered Expression in Lesional Psoriasis
Int. J. Mol. Sci. 2018, 19(10), 2923; https://doi.org/10.3390/ijms19102923 - 26 Sep 2018
Cited by 2
Abstract
Psoriasis is a chronic inflammatory skin disease for which no cure has emerged. Its complex etiology requires the development of an in vitro model representative of the pathology. In this study, we exploited gene profiling analyses on microarray in order to characterize and [...] Read more.
Psoriasis is a chronic inflammatory skin disease for which no cure has emerged. Its complex etiology requires the development of an in vitro model representative of the pathology. In this study, we exploited gene profiling analyses on microarray in order to characterize and further optimize the production of a human psoriatic skin model representative of this in vivo skin disease. Various skin substitutes were produced by tissue-engineering using biopsies from normal, healthy donors, or from lesional or non-lesional skin samples from patients with psoriasis, and their gene expression profiles were examined by DNA microarray. We demonstrated that more than 3540 and 1088 genes (two-fold change) were deregulated between healthy/lesional and lesional/non-lesional psoriatic substitutes, respectively. Moreover, several genes related to lipid metabolism, such as PLA2G4E and PLA2G4C, were identified as repressed in the lesional substitutes. In conclusion, gene profiling analyses identified a list of deregulated candidate genes associated with various metabolic pathways that may contribute to the progression of psoriasis. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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Open AccessArticle
Oxidized Low-Density Lipoprotein-Deteriorated Psoriasis Is Associated with the Upregulation of Lox-1 Receptor and Il-23 Expression In Vivo and In Vitro
Int. J. Mol. Sci. 2018, 19(9), 2610; https://doi.org/10.3390/ijms19092610 - 03 Sep 2018
Cited by 2
Abstract
Psoriasis is a chronic inflammatory skin disease. Even though scientists predict that abnormalities in lipid metabolism play an important role in the pathogenesis of psoriasis, the actual underlying mechanisms are still unclear. Therefore, understanding the possible relationship between mechanisms of the occurrence of [...] Read more.
Psoriasis is a chronic inflammatory skin disease. Even though scientists predict that abnormalities in lipid metabolism play an important role in the pathogenesis of psoriasis, the actual underlying mechanisms are still unclear. Therefore, understanding the possible relationship between mechanisms of the occurrence of psoriasis and dyslipidemia is an important issue that may lead to the development of effective therapies. Under this principle, we investigated the influences of hyperlipidemia in imiquimod (IMQ)-induced psoriasis-like B6.129S2-Apoetm1Unc/J mice and oxidized low-density lipoprotein (oxLDL) in tumor necrosis factor (TNF)-α-stimulated Hacat cells. In our study, we showed that a high-cholesterol diet aggravated psoriasis-like phenomena in IMQ-treated B6.129S2-Apoetm1Unc/J mice. In vitro analysis showed that oxLDL increased keratinocyte migration and lectin-type oxLDL receptor 1 (LOX-1) expression. Evidence suggested that interleukin (IL)-23 was a main cytokine in the pathogenesis of psoriasis. High-cholesterol diet aggravated IL-23 expression in IMQ-treated B6.129S2-Apoetm1Unc/J mice, and oxLDL induced IL-23 expression mediated by LOX-1 in TNF-α-stimulated Hacat cells. Therefore, it will be interesting to investigate the factors for the oxLDL induction of LOX-1 in psoriasis. LOX-1 receptor expression may be another novel treatment option for psoriasis and might represent the most promising strategy. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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Review

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Open AccessReview
The Significance of IL-36 Hyperactivation and IL-36R Targeting in Psoriasis
Int. J. Mol. Sci. 2019, 20(13), 3318; https://doi.org/10.3390/ijms20133318 - 05 Jul 2019
Cited by 6
Abstract
Psoriasis is an immune-mediated inflammatory skin disease that involves mainly T helper (Th)17, Th1 and Th22 lymphocytes, which cause hyper-proliferation of the epidermis with aberrant differentiation of keratinocytes, and local production of chemokines and cytokines. These fuel a self-amplifying loop where these products [...] Read more.
Psoriasis is an immune-mediated inflammatory skin disease that involves mainly T helper (Th)17, Th1 and Th22 lymphocytes, which cause hyper-proliferation of the epidermis with aberrant differentiation of keratinocytes, and local production of chemokines and cytokines. These fuel a self-amplifying loop where these products act on T cells to perpetuate cutaneous inflammatory processes. Among the various inflammatory mediators involved, interleukin (IL)-36 cytokines are important for the recruitment and activation of neutrophils and Th17 cells in psoriatic skin. In particular, IL-36s induce chemokines and cytokines interfere with differentiation/cornification programs in the epidermis, as well as promote pathological angiogenesis and endothelial cell activation. IL-36 cytokines belong to the IL-1 family, and comprise IL-36α, IL-36β, and IL-36γ agonists as well as IL-36 receptor antagonist and IL-38 antagonists. IL-36 cytokines are up-regulated in psoriatic epidermis, and their expression is strongly induced by TNF-α and IL-17. Contrarily, IL-38 antagonist is downregulated, and its impaired expression may be relevant to the dysregulated inflammatory processes induced by IL-36. Here, we discuss on the pathogenic mechanisms leading to the altered balance of IL-36 agonists/antagonists and the significance of this dysregulation in psoriasis. Collection of the information will provide a theoretical basis for the development of novel therapeutic strategies based on IL-36 agonist/antagonist manipulation in psoriasis. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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Open AccessReview
Proteomics in Psoriasis
Int. J. Mol. Sci. 2019, 20(5), 1141; https://doi.org/10.3390/ijms20051141 - 06 Mar 2019
Cited by 2
Abstract
Psoriasis has been thought to be driven primarily by innate and adaptive immune systems that can be modified by genetic and environmental factors. Complex interplay between inflammatory cytokines and T-cells, especially Th1 and Th17 cells, leads to abnormal cell proliferation and psoriatic skin [...] Read more.
Psoriasis has been thought to be driven primarily by innate and adaptive immune systems that can be modified by genetic and environmental factors. Complex interplay between inflammatory cytokines and T-cells, especially Th1 and Th17 cells, leads to abnormal cell proliferation and psoriatic skin lesions. Nevertheless, such mechanisms do not entirely represent the pathogenesis of psoriasis. Moreover, earlier and better biomarkers in diagnostics, prognostics, and monitoring therapeutic outcomes of psoriasis are still needed. During the last two decades, proteomics (a systematic analysis of proteins for their identities, quantities, and functions) has been widely employed to psoriatic research. This review summarizes and discusses all of the previous studies that applied various modalities of proteomics technologies to psoriatic skin disease. The data obtained from such studies have led to (i) novel mechanisms and new hypotheses of the disease pathogenesis; (ii) biomarker discovery for diagnostics and prognostics; and (iii) proteome profiling for monitoring treatment efficacy and drug-induced toxicities. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
Open AccessReview
Advances in Understanding the Immunological Pathways in Psoriasis
Int. J. Mol. Sci. 2019, 20(3), 739; https://doi.org/10.3390/ijms20030739 - 10 Feb 2019
Cited by 14
Abstract
Psoriasis vulgaris is a chronic, immune-mediated, inflammatory, polygenic skin disorder affecting approximately 2% of the population. It has a great impact on quality of life; patients often experience depression, anxiety, stigma as well as suicidal behavior. Even though psoriasis is one of the [...] Read more.
Psoriasis vulgaris is a chronic, immune-mediated, inflammatory, polygenic skin disorder affecting approximately 2% of the population. It has a great impact on quality of life; patients often experience depression, anxiety, stigma as well as suicidal behavior. Even though psoriasis is one of the most studied dermatological conditions, the pathogenesis of the disease is still not completely elucidated. The complex interactions between keratinocytes, dendritic cells, T-lymphocytes, neutrophils and mast cells are responsible for the histopathological changes seen in psoriasis. The pathogenic model leading to the formation of psoriatic plaques has however evolved a lot over the years. There is now enough evidence to support the role of interleukin (IL) -23, IL-17, IL-22, T helper (Th) -17 cells, Th-22 cells, T regulatory cells, transforming growth factor (TGF)-β1 and IL-10 in the pathogenesis of the disease. Moreover, several inflammatory and anti-inflammatory molecules are currently being investigated, some of them showing promising results. The aim of this paper is to look over the most recent advances in the immunological pathways involved in the pathogenesis of psoriasis vulgaris. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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Open AccessCorrection
Correction: Bocheńska, K. et al. Lysosome Alterations in the Human Epithelial Cell Line HaCaT and Skin Specimens: Relevance to Psoriasis. Int. J. Mol. Sci. 2019, 20, 2255
Int. J. Mol. Sci. 2020, 21(2), 594; https://doi.org/10.3390/ijms21020594 - 16 Jan 2020
Abstract
The authors wish to make the following corrections to this paper [...] Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pathology of Psoriasis)
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