Effects of Expression of Transcriptional Factor AP-1 FOSL1 Gene on Psoriatic Process

Соболев, В. В.; Zolotorenko, A. D.; Соболева, А. Г.; Elkin, Amanda; Il’ina, S. A.; Серов, Д. Н.; Потекаев, Н. Н.; Ткаченко, С. Б.; Миннибаев, М. Т.; Piruzyan, A. L.

doi:10.1007/s10517-011-1208-0

Cited by 21 publications

(15 citation statements)

References 12 publications

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“…In contrast one factor, FOSL1, exclusively upregulates progenitor genes while downregulating genes in all three differentiation signatures. Combined with the finding that FOSL1 is upregulated in psoriatic epidermis [30], these results suggest that FOSL1 promotes keratinocyte proliferation. Also, a significant subset of factors, including CREB5, STAT1 and FOS, is associated with activation of early differentiation genes, suggesting these factors are early initiators of epidermal differentiation.…”

Section: Resultssupporting

confidence: 60%

GRHL3 binding and enhancers rearrange as epidermal keratinocytes transition between functional states

et al. 2017

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Transcription factor binding, chromatin modifications and large scale chromatin re-organization underlie progressive, irreversible cell lineage commitments and differentiation. We know little, however, about chromatin changes as cells enter transient, reversible states such as migration. Here we demonstrate that when human progenitor keratinocytes either differentiate or migrate they form complements of typical enhancers and super-enhancers that are unique for each state. Unique super-enhancers for each cellular state link to gene expression that confers functions associated with the respective cell state. These super-enhancers are also enriched for skin disease sequence variants. GRHL3, a transcription factor that promotes both differentiation and migration, binds preferentially to super-enhancers in differentiating keratinocytes, while during migration, it binds preferentially to promoters along with REST, repressing the expression of migration inhibitors. Key epidermal differentiation transcription factor genes, including GRHL3, are located within super-enhancers, and many of these transcription factors in turn bind to and regulate super-enhancers. Furthermore, GRHL3 represses the formation of a number of progenitor and non-keratinocyte super-enhancers in differentiating keratinocytes. Hence, chromatin relocates GRHL3 binding and enhancers to regulate both the irreversible commitment of progenitor keratinocytes to differentiation and their reversible transition to migration.

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Section: Resultssupporting

confidence: 60%

GRHL3 binding and enhancers rearrange as epidermal keratinocytes transition between functional states

et al. 2017

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“…Among epidermal PP-increased DEGs, we identified nine AP-1 binding sites significantly enriched in 2 KB upstream regions (Figure 5). Additionally, in bulk skin biopsies and in LCM-dissected epidermis, expression of genes encoding AP-1 components was significantly altered (e.g., JUNB , FOSL1 and FOS ; Additional file 10) [55,56]. These same AP-1 sites, moreover, were similarly enriched in upstream regions of genes induced by IL-17A in KC cultures (also IFN-γ, TNF, IL-20, IL-22 and IL-24; see Figure 5).…”

Section: Discussionmentioning

confidence: 99%

Dissecting the psoriasis transcriptome: inflammatory- and cytokine-driven gene expression in lesions from 163 patients

et al. 2013

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BackgroundPsoriasis lesions are characterized by large-scale shifts in gene expression. Mechanisms that underlie differentially expressed genes (DEGs), however, are not completely understood. We analyzed existing datasets to evaluate genome-wide expression in lesions from 163 psoriasis patients. Our aims were to identify mechanisms that drive differential expression and to characterize heterogeneity among lesions in this large sample.ResultsWe identified 1233 psoriasis-increased DEGs and 977 psoriasis-decreased DEGs. Increased DEGs were attributed to keratinocyte activity (56%) and infiltration of lesions by T-cells (14%) and macrophages (11%). Decreased DEGs, in contrast, were associated with adipose tissue (63%), epidermis (14%) and dermis (4%). KC/epidermis DEGs were enriched for genes induced by IL-1, IL-17A and IL-20 family cytokines, and were also disproportionately associated with AP-1 binding sites. Among all patients, 50% exhibited a heightened inflammatory signature, with increased expression of genes expressed by T-cells, monocytes and dendritic cells. 66% of patients displayed an IFN-γ-strong signature, with increased expression of genes induced by IFN-γ in addition to several other cytokines (e.g., IL-1, IL-17A and TNF). We show that such differences in gene expression can be used to differentiate between etanercept responders and non-responders.ConclusionsPsoriasis DEGs are partly explained by shifts in the cellular composition of psoriasis lesions. Epidermal DEGs, however, may be driven by the activity of AP-1 and cellular responses to IL-1, IL-17A and IL-20 family cytokines. Among patients, we uncovered a range of inflammatory- and cytokine-associated gene expression patterns. Such patterns may provide biomarkers for predicting individual responses to biologic therapy.

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“…Table S6). All of them involves in regulating immunity and inflammation, which contributes to psoriasis [21][22][23]. The details of hsa_circ_0061012, hsa_circ_0069260, hsa_ circ_0022697, hsa_circ_0043804, hsa_circ_0031329, and hsa_ circ_0062533 were shown in Table 4.…”

Section: Predication Of Common Mres Of Differentially Expressed Circrmentioning

confidence: 99%

Circular RNA Expression Profile and Analysis of Their Potential Function in Psoriasis

Qiao¹,

Ding²,

Yan³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Circular RNAs (circRNAs) are evolutionary conserved circular non-coding RNAs that play a role in several diseases by sequestering (sponging) microRNAs (miRNAs). However, their role in psoriasis remains unclear. In the present study, we investigated the expression of circRNAs and analyzed their potential functions in psoriasis. Methods: The SBC human ceRNA array V1.0 was used to analyze circRNA expression in psoriatic lesions and normal healthy skin tissues. Functional analyses were performed using Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Putative miRNA response elements (MREs) were identified using miRNA target prediction software. Six upregulated circRNAs were verified by quantitative real-time reverse transcription polymerase chain reaction in psoriatic lesions and healthy skin tissues. Results: A total of 4956 circRNAs (3016 upregulated and 1940 downregulated; fold change ≥2 and p< 0.05) were identified as differentially expressed in psoriasis. Furthermore, 4405 MREs were identified among the differentially expressed circRNAs. hsa_circ_0061012 was upregulated in psoriatic lesions compared with normal healthy skin tissues. The top five MREs of hsa_circ_0061012 were hsa-miR-7157-5p, hsa-miR-4769-3p, hsa-miR-6817-5p, hsa-miR-4310, and hsa-miR-6882-3p. GO analysis was carried out to investigate the biological functions enriched among the upregulated targets of five miRNAs in psoriasis. The GO analysis identified that most of top 30 of GO enrichment are related to psoriasis. Conclusion: hsa_circ_0061012 might be a candidate biomarker for psoriasis. The results provide a new perspective for a better understanding of ceRNA-mediated gene regulation in psoriasis, and provide a novel theoretical basis for further studies on the function of circRNA in psoriasis.

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Effects of Expression of Transcriptional Factor AP-1 FOSL1 Gene on Psoriatic Process

Cited by 21 publications

References 12 publications

GRHL3 binding and enhancers rearrange as epidermal keratinocytes transition between functional states

GRHL3 binding and enhancers rearrange as epidermal keratinocytes transition between functional states

Dissecting the psoriasis transcriptome: inflammatory- and cytokine-driven gene expression in lesions from 163 patients

Circular RNA Expression Profile and Analysis of Their Potential Function in Psoriasis

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