NcRNA expression profile in keratinocytes of patients with psoriasis vulgaris
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ABSTRACT:
PROVIDER: PRJNA609557 | ENA |
REPOSITORIES: ENA
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Project description:The aim of our study was to explore lncRNA expression profile in keratinocytes of patients with psoriasis vulgaris to provide new insights into psoriasis.
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Project description:There is a controversy surrounding the existence of palmoplantar pustulosis (PPP) and palmoplantar pustular psoriasis (PPPP) as separate clinical entities or as variants of the same clinical entity. We used gene expression microarray to compare gene expression in PPP and PPPP. PPP and PPPP could not be differentiated using gene expression microarray suggesting that they are not distinct clinical entities. Increased expression of GPRIN1, and ADAM23 in keratinocytes suggests that these proteins could be new therapeutic targets for PPP/PPPP. Skin biopsies from subjects with PPP (3), PPPP (6), psoriasis vulgaris (10) and acral skin from normal subjects (7) were analyzed using gene expression microarray. Principal component analysis showed that PPP and PPPP were different from psoriasis vulgaris and normal acral skin. However gene expression of PPP and PPPP clustered together and could not be used to differentiate PPP from PPPP. Gene-wise comparison between PPP and PPPP found no gene to be differentially expressed with a false discovery rate lower than 0.6. Surprisingly we found a higher expression of several genes involved in neural pathways (e.g. GPRIN and ADAM23) in PPP/PPPP as compared to psoriasis vulgaris and normal acral skin. Immunohistochemistry confirmed those findings and showed a keratinocyte localization for those proteins.
2016-06-30 | E-GEOD-80047 | biostudies-arrayexpress
Project description:Psoriasis is chronic skin disease and an important health concern. Traditional Chinese Medicine (TCM) has shown great promise in the treatment of psoriasis. However, the correlation between TCM Syndromes and genomics of psoriasis has not been evaluated. Here, we analyzed gene expression profiling of monocytes from psoriasis vulgaris patients with different TCM syndrome types to reveal the molecular basis of different psoriasis syndromes. Of the 62 cases of psoriasis vulgaris recruited, 16, 23, and 23 cases were of blood-heat syndrome, blood stasis syndrome, and blood-dryness syndrome, respectively; 10 healthy controls were recruited as controls. Affymertix's Gene Chip ®clariom D gene chip was used to detect the gene expression profile of peripheral blood monocytes collected from recruited individuals. Compared with the healthy control group, 1570 genes were up-regulated and 977 genes were down-regulated in the psoriasis vulgaris patients group; 798 genes and 108 genes were up- and down-regulated in the blood-heat syndrome group respectively; 319 and 433 genes were up- and down-regulated in the blood-dryness syndrome group, respectively; and 502 and 179 genes were up-and down-regulated in the blood-stasis syndrome group. Our analyses indicated not only common differential genes and pathways between psoriasis syndrome groups and healthy controls, but also syndrome-specific genes and pathways. The results of this study link the three syndromes at the gene level and will be useful for clarifying the molecular basis of TCM syndromes of psoriasis. Trial registration: ChiCTR, ChiCTR-TRC-14005185. Registered 8 August 2014, http://www.chictr.org.cn/showproj.aspx?proj=4390 Keywords: Gene chip, Gene expression, Psoriasis vulgaris, TCM syndrome type
2022-02-08 | GSE192867 | GEO
Project description:Optimizing single-cell transcriptomic discrimination of atopic dermatitis versus psoriasis vulgaris
| EGAS00001007487 | EGA
Project description:To identify the gene expression in the peripheral edge of the lesional (PE) skin of psoriasis vulgaris. Methods: Full-thickness skin biopsies of PE skin and uninvolved skin were taken from psoriasis patients. Transcriptomic profiling was constructed by high-throughput next-generation sequencing (NGS) technology. Result: A total of 1,202 DEGs were identified. Of these, 653 (54%) were upregulated and 549 (46%) were downregulated. These DEGs might play a pivotal role in psoriasis pathogenesis. This study accelerates psoriasis-associated gene discovery in the whole picture of PE skin.
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Project description:FelixGarza2017 - Blue Light Treatment of
Psoriasis (simplified)
This model is described in the article:
A Dynamic Model for
Prediction of Psoriasis Management by Blue Light
Irradiation.
Félix Garza ZC, Liebmann J,
Born M, Hilbers PA, van Riel NA.
Front Physiol 2017; 8: 28
Abstract:
Clinical investigations prove that blue light irradiation
reduces the severity of psoriasis vulgaris. Nevertheless, the
mechanisms involved in the management of this condition remain
poorly defined. Despite the encouraging results of the clinical
studies, no clear guidelines are specified in the literature
for the irradiation scheme regime of blue light-based therapy
for psoriasis. We investigated the underlying mechanism of blue
light irradiation of psoriatic skin, and tested the hypothesis
that regulation of proliferation is a key process. We
implemented a mechanistic model of cellular epidermal dynamics
to analyze whether a temporary decrease of keratinocytes
hyper-proliferation can explain the outcome of phototherapy
with blue light. Our results suggest that the main effect of
blue light on keratinocytes impacts the proliferative cells.
They show that the decrease in the keratinocytes proliferative
capacity is sufficient to induce a transient decrease in the
severity of psoriasis. To study the impact of the therapeutic
regime on the efficacy of psoriasis treatment, we performed
simulations for different combinations of the treatment
parameters, i.e., length of treatment, fluence (also referred
to as dose), and intensity. These simulations indicate that
high efficacy is achieved by regimes with long duration and
high fluence levels, regardless of the chosen intensity. Our
modeling approach constitutes a framework for testing diverse
hypotheses on the underlying mechanism of blue light-based
phototherapy, and for designing effective strategies for the
treatment of psoriasis.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000695.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
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Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000695 | BioModels
Project description:Psoriasis is a chronic inflammatory skin disease characterized by marked proliferation of keratinocytes leading to pronounced epidermal hyperplasia, elongation of rete ridges and hyperkeratosis. The most common form of psoriasis, chronic plaque psoriasis (Psoriasis vulgaris), involves relatively stable occurrence and progression of sharply demarcated lesions, usually on the trunk and extremities, which share a combination of trademark histological features, including tortuous and dilated dermal capillaries, loss of the epidermal granular layer, and accumulation of neutrophils beneath parakeratotic scale. In this study, whole-genome transcriptional profiling was used to characterize gene expression in 4 lesional and uninvolved skin samples obtained from patients with stable chronic plaque psoriasis. Skin mRNA expression was analysed by microarray. Four individuals with chronic plaque psoriasis were enrolled. 6 mm punch biopsies were obtained under local anaesthesia (lidocaine) from uninvolved skin and a target plaque.
2013-12-10 | E-GEOD-50790 | biostudies-arrayexpress
Project description:Psoriasis is a common chronic inflammatory skin disease. Keratinocytes (KCs) are important effector cells that can recruit inflammatory cells by releasing inflammatory factors and chemokines to promote the inflammatory cascade in psoriasis. However, the mechanism underlying KC activation in psoriasis remains unclear. Livin is an inhibitor of apoptotic proteins and its expression can directly affect the proliferation and metastasis of tumor cells. Livin expression has been reported to be significantly increased in the lesions of patients with psoriasis; however, its specific role in KC activation has not yet been reported. The aim of this study was to investigate whether livin regulates KC activation and causes the release of inflammatory mediators. The expression levels of livin in patients with psoriasis, an imiquimod (IMQ) mouse model, and M5-treated HaCaT cells were determined via immunofluorescence staining, reverse transcription-quantitative polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA), and western blotting. We constructed livin knockdown (Knockdown-HaCaT) and negative control (NC-HaCaT) cells using human immunodeficiency virus-1-based lentiviral vectors to study the function of livin in KCs via RNA-sequencing and proteomics analysis. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. Moreover, the effect of livin expression on the release of inflammatory mediators in KCs was verified using ELISA.
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Project description:Psoriasis is characterized by hyperplasia and disrupted differentiation of keratinocytes. Keratinocytes are considered not only the target but also the critical participants. To explore the role of keratinocytes in psoriasis, we used microarrays to compared gene expression profile of epidermis between psoriasis lesions and healthy normal skin.
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