Letteratura scientifica selezionata sul tema "PSORIASIS SIGNATURE GENES"
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Articoli di riviste sul tema "PSORIASIS SIGNATURE GENES"
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Abdallah, Florence, Elodie Henriet, Amandine Suet, Ali Arar, Rudy Clemençon, Jean-Marc Malinge, Gaël Lecellier, Patrick Baril e Chantal Pichon. "miR-21-3p/IL-22 Axes Are Major Drivers of Psoriasis Pathogenesis by Modulating Keratinocytes Proliferation-Survival Balance and Inflammatory Response". Cells 10, n. 10 (26 settembre 2021): 2547. http://dx.doi.org/10.3390/cells10102547.
Testo completoAbstract (sommario):
Psoriasis is a chronic inflammatory skin disease that is mediated by complex crosstalk between immune cells and keratinocytes (KCs). Emerging studies have showed a specific psoriatic microRNAs signature, in which miR-21 is one of the most upregulated and dynamic miRNAs. In this study, we focused our investigations on the passenger miR-21-3p strand, which is poorly studied in skin and in psoriasis pathogenesis. Here, we showed the upregulation of miR-21-3p in an IMQ-induced psoriasiform mouse model. This upregulation was correlated with IL-22 expression and functionality, both in vitro and in vivo, and it occurred via STAT3 and NF-κB signaling. We identified a network of differentially expressed genes involved in abnormal proliferation control and immune regulatory genes implicated in the molecular pathogenesis of psoriasis in response to miR-21-3p overexpression in KCs. These results were confirmed by functional assays that validated the proliferative potential of miR-21-3p. All these findings highlight the importance of miR-21-3p, an underestimated miRNA, in psoriasis and provide novel molecular targets for therapeutic purposes.
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Kvist-Hansen, Amanda, Hannah Kaiser, Xing Wang, Martin Krakauer, Peter Michael Gørtz, Benjamin D. McCauley, Claus Zachariae, Christine Becker, Peter Riis Hansen e Lone Skov. "Neutrophil Pathways of Inflammation Characterize the Blood Transcriptomic Signature of Patients with Psoriasis and Cardiovascular Disease". International Journal of Molecular Sciences 22, n. 19 (6 ottobre 2021): 10818. http://dx.doi.org/10.3390/ijms221910818.
Testo completoAbstract (sommario):
Background: Patients with psoriasis have an increased risk of atherosclerotic cardiovascular disease (CVD). The molecular mechanisms behind this connection are not fully understood, but the involvement of neutrophils have drawn attention as a shared inflammatory factor. Methods: RNA sequencing using the Illumina platform was performed on blood from 38 patients with moderate to severe psoriasis; approximately half had prior CVD. The neutrophil to lymphocyte ratio (NLR) was obtained from blood samples. Subclinical atherosclerosis was assessed by 18F-fluorodeoxyglucose positron emission tomography/computed tomography and ultrasound imaging. Transcriptomic analysis for differential expression and functional enrichment were performed, followed by correlation analyses of differentially expressed genes (DEGs), NLR and subclinical measurers of CVD. Results: 291 genes were differentially expressed between patients with psoriasis with and without CVD. These included 208 upregulated and 83 downregulated DEGs. Neutrophil degranulation was identified as the most significant process related to the upregulated DEGs. Genes for the neutrophil-associated markers MPO, MMP9, LCN2, CEACAM1, CEACAM6 and CEACAM8 were identified as being of special interest and their mRNA levels correlated with NLR, high-sensitive C-reactive protein and markers of subclinical CVD. Conclusions: Patients with psoriasis and CVD had an increased expression of genes related to neutrophil degranulation in their blood transcriptome compared with patients with psoriasis without CVD. NLR may be a potential biomarker of subclinical CVD in psoriasis.
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West, Peter W., Chiara Tontini, Haris Atmoko, Orsolya Kiss, Terence Garner, Rajia Bahri, Richard B. Warren, Christopher E. M. Griffiths, Adam Stevens e Silvia Bulfone-Paus. "Human Mast Cells Upregulate Cathepsin B, a Novel Marker of Itch in Psoriasis". Cells 12, n. 17 (30 agosto 2023): 2177. http://dx.doi.org/10.3390/cells12172177.
Testo completoAbstract (sommario):
Mast cells (MCs) contribute to skin inflammation. In psoriasis, the activation of cutaneous neuroimmune networks commonly leads to itch. To dissect the unique contribution of MCs to the cutaneous neuroinflammatory response in psoriasis, we examined their density, distribution, relation to nerve fibres and disease severity, and molecular signature by comparing RNA-seq analysis of MCs isolated from the skin of psoriasis patients and healthy volunteers. In involved psoriasis skin, MCs and Calcitonin Gene-Related Peptide (CGRP)-positive nerve fibres were spatially associated, and the increase of both MC and nerve fibre density correlated with disease severity. Gene set enrichment analysis of differentially expressed genes in involved psoriasis skin showed significant representation of neuron-related pathways (i.e., regulation of neuron projection along with dendrite and dendritic spine morphogenesis), indicating MC engagement in neuronal development and supporting the evidence of close MC–nerve fibre interaction. Furthermore, the analysis of 208 identified itch-associated genes revealed that CTSB, TLR4, and TACR1 were upregulated in MCs in involved skin. In both whole-skin published datasets and isolated MCs, CTSB was found to be a reliable indicator of the psoriasis condition. Furthermore, cathepsin B+ cells were increased in psoriasis skin and cathepsin B+ MC density correlated with disease severity. Therefore, our study provides evidence that cathepsin B could serve as a common indicator of the MC-dependent itch signature in psoriasis.
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Tapak, Leili, Saeid Afshar, Mahlagha Afrasiabi, Mohammad Kazem Ghasemi e Pedram Alirezaei. "Application of Genetic Algorithm-Based Support Vector Machine in Identification of Gene Expression Signatures for Psoriasis Classification: A Hybrid Model". BioMed Research International 2021 (8 settembre 2021): 1–10. http://dx.doi.org/10.1155/2021/5520710.
Testo completoAbstract (sommario):
Background. Psoriasis is a chronic autoimmune disease impairing significantly the quality of life of the patient. The diagnosis of the disease is done via a visual inspection of the lesional skin by dermatologists. Classification of psoriasis using gene expression is an important issue for the early and effective treatment of the disease. Therefore, gene expression data and selection of suitable gene signatures are effective sources of information. Methods. We aimed to develop a hybrid classifier for the diagnosis of psoriasis based on two machine learning models of the genetic algorithm and support vector machine (SVM). The method also conducts gene signature selection. A publically available gene expression dataset was used to test the model. Results. A number of 181 probe sets were selected among the original 54,675 probes using the hybrid model with a prediction accuracy of 100% over the test set. A number of 10 hub genes were identified using the protein-protein interaction network. Nine out of 10 identified genes were found in significant modules. Conclusions. The results showed that the genetic algorithm improved the SVM classifier performance significantly implying the ability of the proposed model in terms of detecting relevant gene expression signatures as the best features.
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Krishnan, Vidya S., e Sulev Kõks. "Transcriptional Basis of Psoriasis from Large Scale Gene Expression Studies: The Importance of Moving towards a Precision Medicine Approach". International Journal of Molecular Sciences 23, n. 11 (30 maggio 2022): 6130. http://dx.doi.org/10.3390/ijms23116130.
Testo completoAbstract (sommario):
Transcriptome profiling techniques, such as microarrays and RNA sequencing (RNA-seq), are valuable tools for deciphering the regulatory network underlying psoriasis and have revealed large number of differentially expressed genes in lesional and non-lesional skin. Such approaches provide a more precise measurement of transcript levels and their isoforms than any other methods. Large cohort transcriptomic analyses have greatly improved our understanding of the physiological and molecular mechanisms underlying disease pathogenesis and progression. Here, we mostly review the findings of some important large scale psoriatic transcriptomic studies, and the benefits of such studies in elucidating potential therapeutic targets and biomarkers for psoriasis treatment. We also emphasised the importance of looking into the alternatively spliced RNA isoforms/transcripts in psoriasis, rather than focussing only on the gene-level annotation. The neutrophil and blood transcriptome signature in psoriasis is also briefly reviewed, as it provides the immune status information of patients and is a less invasive platform. The application of precision medicine in current management of psoriasis, by combining transcriptomic data, improves the clinical response outcome in individual patients. Drugs tailored to individual patient’s genetic profile will greatly improve patient outcome and cost savings for the healthcare system.
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Golden, Jackelyn, Brian Richardson, Divya Seth, Michael Cartwright, Rafick-Pierre Sekaly, Thomas S. McCormick, Kevin D. Cooper, Cheryl M. Cameron e Mark J. Cameron. "Transcriptomic meta-analysis reveals signatures of chronic inflammation in the classical monocyte population". Journal of Immunology 200, n. 1_Supplement (1 maggio 2018): 42.25. http://dx.doi.org/10.4049/jimmunol.200.supp.42.25.
Testo completoAbstract (sommario):
Abstract Individuals with chronic diseases are reported to have increased classical monocytes (CD14++CD16neg) which can be activated by an infectious agent and/or inflammatory milieu. Both psoriasis and HIV are considered chronic inflammatory diseases and affected individuals display alterations in monocyte phenotype and function. Moreover, individuals with either psoriasis or HIV demonstrate a significantly increased risk of developing cardiovascular disease (CVD). We sorted classical monocytes from psoriatic and healthy controls and compared them to classical monocytes from PLHIV individuals (elite controllers (EC) and non-controllers (NC, cART suppressed). Using RNA-Seq, we identified significant differentially expressed genes (DEG, p<0.05) in psoriasis monocytes (164 DEGs; compared to controls) and in HIV+ classical monocytes from ECs (540 DEGs; compared to NC). We then performed a meta-analysis of the psoriasis transcriptome to the EC-HIV+ transcriptome, revealing a common set of DEGs comprising a unique gene signature involving cellular stress, chemokines, adhesion, and the clotting cascade. We further analyzed the common DEGs via pathway analysis (p & false discovery rate<0.05) and STRING analysis to reveal a common dysregulated network of DEG between psoriasis and HIV. Importantly, we identified a focused network of DEG that may hallmark chronic inflammation in monocyte phenotypes. Therefore, our transcriptional meta-analysis identified candidate biomarkers that may underlie common pathologic mechanisms in psoriasis and HIV and serve as highly refined targets to treat not only primary disease, but also associated comorbidities (e.g. CVD) related to inflammation.
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Lu, Chih-Hao, Chao-Yang Lai, Da-Wei Yeh, Yi-Ling Liu, Yu-Wen Su, Li-Chung Hsu, Chung-Hsing Chang, S. L. Catherine Jin e Tsung-Hsien Chuang. "Involvement of M1 Macrophage Polarization in Endosomal Toll-Like Receptors Activated Psoriatic Inflammation". Mediators of Inflammation 2018 (16 dicembre 2018): 1–14. http://dx.doi.org/10.1155/2018/3523642.
Testo completoAbstract (sommario):
Psoriasis is a chronic inflammatory skin disorder that affects ~2%–3% of the worldwide population. Inappropriate and excessive activation of endosomal Toll-like receptors 7, 8, and 9 (TLRs 7–9) at the psoriatic site has been shown to play a pathogenic role in the onset of psoriasis. Macrophage is a major inflammatory cell type that can be differentiated into phenotypes M1 and M2. M1 macrophages produce proinflammatory cytokines, and M2 macrophages produce anti-inflammatory cytokines. The balance between these two types of macrophages determines the progression of various inflammatory diseases; however, whether macrophage polarization plays a role in psoriatic inflammation activated by endosomal TLRs has not been investigated. In this study, we investigated the function and mechanism of macrophages related to the pathogenic role of TLRs 7–9 in the progression of psoriasis. Analysis of clinical data in database revealed significantly increased expression of macrophage markers and inflammatory cytokines in psoriatic tissues over those in normal tissues. In animal studies, depletion of macrophages in mice ameliorated imiquimod, a TLR 7 agonist-induced psoriatic response. Imiquimod induced expression of genes and cytokines that are signature of M1 macrophage in the psoriatic lesions. In addition, treatment with this TLR 7 agonist shifted macrophages in the psoriatic lesions to a higher M1/M2 ratio. Both of the exogenous and endogenous TLR 7–9 ligands activated M1 macrophage polarization. M1 macrophages expressed higher levels of proinflammatory cytokines and TLRs 7–9 than M2 macrophages. These results suggest that by rendering macrophages into a more inflammatory status and capable of response to their ligands in the psoriatic sites, TLR 7–9 activation drives them to participate in endosomal TLR-activated psoriatic inflammation, resulting in an amplified inflammatory response. Our results also suggest that blocking M1 macrophage polarization could be a strategy which enables inhibition of psoriatic inflammation activated by these TLRs.
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Choudhary, Saumya, Dibyabhaba Pradhan, Noor S. Khan, Harpreet Singh, George Thomas e Arun K. Jain. "Decoding Psoriasis: Integrated Bioinformatics Approach to Understand Hub Genes and Involved Pathways". Current Pharmaceutical Design 26, n. 29 (4 settembre 2020): 3619–30. http://dx.doi.org/10.2174/1381612826666200311130133.
Testo completoAbstract (sommario):
Background: Psoriasis is a chronic immune mediated skin disorder with global prevalence of 0.2- 11.4%. Despite rare mortality, the severity of the disease could be understood by the accompanying comorbidities, that has even led to psychological problems among several patients. The cause and the disease mechanism still remain elusive. Objective: To identify potential therapeutic targets and affecting pathways for better insight of the disease pathogenesis. Method: The gene expression profile GSE13355 and GSE14905 were retrieved from NCBI, Gene Expression Omnibus database. The GEO profiles were integrated and the DEGs of lesional and non-lesional psoriasis skin were identified using the affy package in R software. The Kyoto Encyclopaedia of Genes and Genomes pathways of the DEGs were analyzed using clusterProfiler. Cytoscape, V3.7.1 was utilized to construct protein interaction network and analyze the interactome map of candidate proteins encoded in DEGs. Functionally relevant clusters were detected through Cytohubba and MCODE. Results: A total of 1013 genes were differentially expressed in lesional skin of which 557 were upregulated and 456 were downregulated. Seven dysregulated genes were extracted in non-lesional skin. The disease gene network of these DEGs revealed 75 newly identified differentially expressed gene that might have a role in development and progression of the disease. GO analysis revealed keratinocyte differentiation and positive regulation of cytokine production to be the most enriched biological process and molecular function. Cytokines -cytokine receptor was the most enriched pathways. Among 1013 identified DEGs in lesional group, 36 DEGs were found to have altered genetic signature including IL1B and STAT3 which are also reported as hub genes. CCNB1, CCNA2, CDK1, IL1B, CXCL8, MKI 67, ESR1, UBE2C, STAT1 and STAT3 were top 10 hub gene. Conclusion: The hub genes, genomic altered DEGs and other newly identified differentially dysregulated genes would improve our understanding of psoriasis pathogenesis, moreover, the hub genes could be explored as potential therapeutic targets for psoriasis.
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Shalbaf, Mohammad, Adewonuola A. Alase, Anna Berekmeri, Md Yuzaiful Md Yusof, Jelena Pistolic, Mark J. Goodfield, Sara Edward et al. "Plucked hair follicles from patients with chronic discoid lupus erythematosus show a disease-specific molecular signature". Lupus Science & Medicine 6, n. 1 (luglio 2019): e000328. http://dx.doi.org/10.1136/lupus-2019-000328.
Testo completoAbstract (sommario):
ObjectiveWhen faced with clinical symptoms of scarring alopecia—the standard diagnostic pathway involves a scalp biopsy which is an invasive and expensive procedure. This project aimed to assess if plucked hair follicles (HFs) containing living epithelial cells can offer a non-invasive approach to diagnosing inflammatory scalp lesions.MethodsLesional and non-lesional HFs were extracted from the scalp of patients with chronic discoid lupus erythematosus (CDLE), psoriasis and healthy controls. RNA was isolated from plucked anagen HFs and microarray, as well as quantitative real-time PCR was performed.ResultsHere, we report that gene expression analysis of only a small number of HF plucked from lesional areas of the scalp is sufficient to differentiate CDLE from psoriasis lesions or healthy HF. The expression profile from CDLE HFs coincides with published profiles of CDLE from skin biopsy. Genes that were highly expressed in lesional CDLE corresponded to well-known histopathological diagnostic features of CDLE and included those related to apoptotic cell death, the interferon signature, complement components and CD8+ T-cell immune responses.ConclusionsWe therefore propose that information obtained from this non-invasive approach are sufficient to diagnose scalp lupus erythematosus. Once validated in routine clinical settings and compared with other scarring alopecias, this rapid and non-invasive approach will have great potential for paving the way for future diagnosis of inflammatory scalp lesions.
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Sumner, Emma J., Daniel McCluskey, Satveer K. Mahil, Myles Lewis e Francesca Capon. "P17 A signature of IL-36 activation in systemic lupus erythematosus skin". British Journal of Dermatology 189, n. 1 (luglio 2023): e20-e21. http://dx.doi.org/10.1093/bjd/ljad174.038.
Testo completoAbstract (sommario):
Abstract Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with heterogeneous presentation. Joint and kidney disease represent the largest cause of morbidity, and visually distinctive skin complications are often present. While it has long been established that organ damage is caused by autoantibodies forming large immune complexes in the affected tissues, a detailed understanding of disease processes is still lacking. Here, we propose that interleukin (IL)-36 cytokines, which drive cutaneous and systemic symptoms in psoriasis, are also implicated in the pathogenesis of SLE. Given that the IL-36 receptor is prominently expressed in keratinocytes, we investigated this hypothesis in skin. We first carried out a systematic review of SLE single-cell RNA sequencing studies, identifying two data sets (∼50 000 cells in total) generated from patient skin biopsies. We processed both data sets with the same standardized pipeline, using the Seurat package. This identified 10 distinct cell clusters, replicating the cell types described in the original studies and identifying the main cell populations observed in human skin. Subsequent gene expression analysis confirmed that, in both data sets, the expression of IL36G and IL1RL2 (the genes encoding IL-36γ and its receptor) was highest in keratinocytes. Interestingly, subclustering showed that this signal was driven by the expression of IL36G in supraspinous keratinocytes and of IL1RL2 in proliferating keratinocytes. In the first data set, the expression of IL36G and IL1RL2 was readily detectable in lesional keratinocytes but virtually nonexistent in their nonlesional counterparts. A comparison of lesional and nonlesional keratinocytes also identified 297 differentially expressed genes (DEGs; log2 fold change > 1.2, false discovery rate < 0.05) in the first study and 234 in the second. To further explore these findings, we compared the above DEG with a set of 182 genes (previously defined by our group) that are upregulated in IL-36-stimulated keratinocytes. This demonstrated a significant over-representation of the IL-36 signature genes among the DEGs observed in lesional SLE keratinocytes (P < 0.005 in both data sets). These observations indicate that IL-36 is likely to contribute to skin inflammation in SLE, warranting further studies of this cytokine in organs affected by the disease.
Tesi sul tema "PSORIASIS SIGNATURE GENES"
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GANGWAR, PAWAN SINGH. "INTEGRATIVE TRANSCRIPTOME DATA ANALYSIS REVEALS PSORIASIS SIGNATURE GENES AND ITS POTENTIAL ROLE IN DRUG REPURPOSING". Thesis, 2020. http://dspace.dtu.ac.in:8080/jspui/handle/repository/18059.
Testo completoAbstract (sommario):
Expression profiling of gene transcripts had been applied in biomedical researches successfully
for over a decade. Psoriasis being a chronic inflammatory skin disorder have complex
pathological features and unmet pharmacological demands. Therefore, a number of research
studies have identified the genes which are differentially expressed in psoriasis skin as
compared to the control or normal skin. Although, there is a considerable variance in the
differentially expressed gene (DEG) list as reported by several research groups and the precise
cause of psoriasis occurrence is still not understood entirely. In this study, the gene expression
data from three different microarray studies, consisting of 117 samples in total and more than
1,35,000 transcripts, was analysed with the help of a ranking based approach. Subsequently,
the 66 psoriatic gene expression signatures identified in total, were consistently showing
dysregulation across the three studies. Furthermore, functional annotation of the identified
genes implicated their role in skin development, epidermal development, keratinocyte
differentiation, inflammation, immune response, and antimicrobial humoral response. By using
a bioinformatics approach, skin development and keratinocyte differentiation pathway were
identified as most over represented pathways among 66 signature genes. The main role of
keratinocytes is in barrier function due to their presence in the epidermis. An enhanced
understanding of keratinocytes function in psoriasis will prove to be important in developing
novel barrier therapies for the disease. Finally, a framework is presented which identifies
potential drug repositioning opportunities utilising a systemic data-driven approach which
helps to discover association amongst genes, diseases and drugs. Such mechanisms facilitated
potential drug repurposing for psoriasis by identifying and suggesting new indications of
existing drugs.
Capitoli di libri sul tema "PSORIASIS SIGNATURE GENES"
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Bhalla, Parinishtha, Anukriti Verma, Bhawna Rathi, Shivani Sharda e Pallavi Somvanshi. "Exploring Molecular Signatures in Spondyloarthritis: A Step Towards Early Diagnosis". In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 142–55. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_15.
Testo completoAbstract (sommario):
AbstractSpondyloarthritis is an acute inflammatory disorder of the musculoskeletal system often accompanied by pain, stiffness, bone and tissue damage. It majorly consists of ankylosing spondylitis, psoriatic arthritis and reactive arthritis. It follows a differential diagnosis pattern for demarcation between the spondyloarthritis subtypes and other arthritic subtypes such as rheumatoid arthritis, juvenile arthritis and osteoarthritis due to the heterogeneity causing gradual chronicity and complications. Presence of definite molecular markers can not only improve diagnosis efficiency but also aid in their prognosis and therapy. This study is an attempt to compose a refined list of such unique and common molecular signatures of the considered subtypes, by employing a reductionist approach amalgamating gene retrieval, protein-protein interaction network, functional, pathway, micro-RNA-gene and transcription factor-gene regulatory network analysis. Gene retrieval and protein-protein interaction network analysis resulted in unique and common interacting genes of arthritis subtypes. Functional annotation and pathway analysis found vital functions and pathways unique and common in arthritis subtypes. Furthermore, miRNA-gene and transcription factor-gene interaction networks retrieved unique and common miRNA’s and transcription factors in arthritis subtypes. Furthermore, the study identified important signatures of arthritis subtypes that can serve as markers assisting in prognosis, early diagnosis and personalized treatment of arthritis patients requiring validation via prospective experimental studies.