The transcriptomic data of TCN1 overexpression in HaCaT cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE302664 | GEO | 2025/11/27
REPOSITORIES: GEO
Similar Datasets
Project description:The transcriptomic data of TCN1 overexpression in HaCaT cells
| PRJNA1291693 | ENA
Project description:Psoriasis is an inflammatory skin disease and the exact pathogenesis has not been fully illuminated yet. It has been demonstrated that interleukin-22 (IL-22) plays a significant role in the pathogenesis of psoriasis. Our study aimed to explore the role of IL-22 and its target miRNAs in pathogenesis of psoriasis.
2015-08-27 | GSE72396 | GEO
Project description:HaCAT cells were treated with pentafactor (M5) to construct a psoriasis cell model, which was used to study the pathogenesis of psoriasis at the in vitro level. This study aimed to explore the genes activated by pentafactor (M5) treatment.
2026-01-05 | GSE302830 | GEO
Project description:Psoriasis is an inflammatory, IL-17-driven skin disease in which autoantigen-induced CD8+ T cells have been identified as pathogenic drivers. In this study, we used single-cell RNA-seq to identify 11 transcriptionally diverse CD8+ T cell subsets in psoriatic and healthy skin. Among several inflammatory subsets enriched in psoriatic skin, we observed two Tc17 subsets that were metabolically divergent, developmentally related, and expressed CXCL13, which we found to be a biomarker of psoriasis severity. Despite high co-inhibitory receptor expression in the Tc17 clusters, a comparison of these cells with melanoma-infiltrating CD8+ T cells revealed upregulated cytokine, cytolytic, and metabolic transcriptional activity in the psoriatic cells that differed from an exhaustion program. Our findings provide a high-resolution view of cutaneous CD8+ T cells in psoriasis and healthy skin and shed light on their functional distinctions within the chronic pathologies of autoimmunity and cancer.
2021-01-05 | GSE146264 | GEO
Project description:This study aimed to explore the downstream signal pathways by TYMP in keratinocyte hyperproliferation.
2026-04-15 | GSE309584 | GEO
Project description:Epigenetics plays a role in the pathogenesis of psoriasis vulgaris and generalized pustular psoriasis (GPP) through DNA methylation modifications that cause changes in immune responses. Psoriasis vulgaris is dominated by autoimmune responses, driven by Th17 cells producing IL-17, whereas GPP is dominated by autoinflammatory responses resulting from IL-36 dysregulation and neutrophil hyperactivation. Objective: This study aims to determine the DNA methylation profile and analyze the differences in IL-17 and IL-36 levels in both psoriasis phenotypes and healthy controls. Method: This study employed a cross-sectional design, comprising 20 patients with psoriasis vulgaris, three patients with GPP, and 13 healthy controls. DNA methylation profiles were assessed using Reduced Representation Methylation Sequencing, while IL-17 and IL-36 levels were assessed using ELISA. Results: Increased 5-methyl cytosine (5mC) was identified in psoriasis vulgaris and GPP compared to healthy controls. Increased 5mC at the FOXP3 promoter was identified in GPP and psoriasis vulgaris with high IL-17 levels, while decreased 5mC at the CARD14 promoter was identified in psoriasis vulgaris with high IL-17 levels. GPP showed higher IL-17 levels than healthy controls (p<0.05). IL-17 levels in psoriasis vulgaris showed no significant difference compared to GPP and healthy controls (p>0.05). IL-36 levels did not differ significantly among the three groups, with the highest IL-36 levels observed in psoriasis vulgaris (p>0.05). Conclusion: Increased DNA methylation in the FOXP3 gene promoter is predicted to cause high IL- 17 levels in psoriasis vulgaris and GPP, while IL-36 levels are higher only in psoriasis vulgaris.
2025-08-07 | GSE304903 | GEO
Project description:Background: Psoriasis is an inflammatory skin disease associated with systemic inflammation and comorbidities such as diabetes and cardiovascular disease. Although the association between psoriasis and obesity has been studied extensively, the role of cutaneous adipose tissue (CAT) in pathogenesis of psoriasis remains unclear. Objectives This study aimed to provide a comprehensive evaluation of the CAT transcriptome in psoriasis patients and investigate the effects of IL-17 pathway blockade on adipose tissue inflammation. Methods: In this randomized, double-blind, placebo-controlled phase 4 study (ObePso study), CAT biopsies were obtained from lesional (LS-CAT) and non-lesional skin (NL-CAT) of 82 psoriasis patients and 15 healthy controls. Patients were randomized to receive either secukinumab or placebo for 12 weeks. RNA sequencing and subsequent analyses were performed to identify differentially expressed genes and pathways. Results: Psoriatic CAT showed significant gene expression differences compared to controls, with 2132 differentially expressed transcripts identified. Both LS-CAT and NL-CAT exhibited activation of IL-17-induced, antimicrobial peptides-related, and neutrophil degranulation-related pathways. Obesity expanded differential gene expression in psoriasis by more than 100%, suggesting an additive or synergistic interaction between psoriasis and adiposity. Obese psoriasis patients showed activation of pathways related to collagen metabolism, cytokine storm signaling, and IL-17A signaling. Secukinumab treatment significantly improved inflammation in psoriatic CAT, with obese patients showing greater improvement than non-obese patients. Conclusions: This study provides the first comprehensive evaluation of the adipose tissue transcriptome in psoriasis patients. The findings reveal a strong inflammatory signature in psoriatic CAT, which is partly IL-17 dependent. The study also demonstrates that obesity amplifies the inflammatory response in psoriatic adipose tissue. IL-17 blockade with secukinumab significantly improved CAT inflammation, with enhanced benefits observed in obese individuals. These results highlight the potential role of adipose tissue in psoriasis pathogenesis and suggest that targeting adipose tissue inflammation may be a valuable therapeutic approach, particularly in obese psoriasis patients.
2026-01-14 | GSE287022 | GEO
Project description:IL-17 antagonists induce impressive clinical benefit in psoriasis, but it is unknown too what extent cellular and molecular characteristics of psoriasis are suppressed by a clinically relevant dose and schedule of any IL-17 antagonist. Examine the effects the IL-17A receptor antagonist brodalumab, on the clinical and molecular characteristics of psoriasis, including IL-17 dependent gene-sets.
2020-04-02 | GSE117468 | GEO
Project description:The efficacy of monoclonal antibodies against either interleukin (IL)-17 or the IL-17 receptor in psoriasis therapy provides strong evidence that IL-17 is the major inflammatory mediation in this disease. However, how IL-17 induces epidermal hyperplasia in psoriasis remains largely unknown. Here, we show that IL-17 actives NF-kB in keratinocytes and initiates the NF-kB-dependent transcription of microRNA-31 (miR-31), one of the most abundant microRNAs in the epidermis of lesional skin of psoriasis and two related mouse models. Similar to IL-17 deficiency (IL-17-/-), knocking out miR-31 (miR-31-/-) or targeting it by antagomir-31 prevents keratinocytes Ki67 expression and inhibits acanthosis and dermal inflammation in psoriasis mouse model. Moreover, PPP6c, a negative regulator restricting G0/G1 to G2/M phase progression in the cell cycle, is diminished in human psoriatic epidermis and is directly targeted by miR-31. Inhibition of ppp6c is functionally important for the biological effects of miR-31 in the development of epidermal hyperplasia. Thus, our data define IL-17-inducede miR-31 and its target ppp6c as critical factors for hyperproliferative epidermis in psoriasis.
2013-12-31 | GSE50099 | GEO
Project description:Activation of Sirtuin (silent mating type information regulation 2 homolog) 1, or SIRT1, is an unexplored therapeutic approach for treatment of inflammatory diseases. The goal of this study was to evaluate the clinical activity and tolerability of multiple doses of SRT2104, a selective activator of SIRT1, in patients with moderate to severe psoriasis after day 84 of treatment. Forty patients were randomized 4:1 to three escalating doses of SRT2104 (250, 500, 1000 mg/d SRT2104 or placebo). Across all SRT2104 groups, 34.6% of patients (9 out of 26; 90% CI 18.0%-54.2%, p<0.0001) achieved good to excellent histological improvement based on skin biopsies taken at baseline and day 84. To evaluate the changes in expression profile with treatment and to identify pathways involved in histological improvement, a subset of 22 Pre and Post treatment biopsies from 11 patients (4 Placebo, 7 Active Treatment) were hybridized to hgu133plus2 chips. Improvement in histology was associated with modulation of IL-17 and TNF-_ signaling pathways and keratinocyte differentiation target genes. Various studies suggest a crucial role of TNF_ and IL-17 in psoriasis pathogenesis and IL-17/TNF_ synergism induces a strong induction of differentially expressed genes in psoriasis, thus advocating a crucial role of IL-17/TNF_ combination in the molecular basis of disease (Chiricozzi et al., 2010). In the current study, broad scale gene expression profiling revealed that SRT2104 significantly reduced known IL-17 and TNF_ responsive genes including SERPINB4, S100A12, SERPINB3, kynu etc. even though the sample size for this analysis was small. One of the most highly modulated genes by SRT2104 included Kynu, a gene that regulates tryptophan metabolism, known to confer antibacterial effector functions (Daubener and MacKenzie, 1999). Interestingly kynu is part of the etanercept residual genomic profile that is not modulated by etanercept therapy even though clinical efficacy is achieved. Possibly, SRT2104 may be modulating the lipid barrier of the epidermis of psoriatic skin via modulation of keratinocyte diferentiation genes, which would be consistent with the observed improvement in skin histology. These results indicate a combinatorial effect of SRT2104 on TNF_, and IL-17 inflammatory signaling pathways and keratinocyte differentiation that could be a contributing factor towards improvement in clinical scores by the SIRT1 activator, SRT2104. Paired Pre (Day 1) and Post (Day 84) Treatment samples were obtained from 4 Placebo Patients and 7 patients treated with SRT2104 at 3 different doses (250, 500, 1000 mg).
2014-11-12 | E-GEOD-50614 | biostudies-arrayexpress