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Expression data from IMQ-induced psoriasis-like skin inflammation in miR-146a-/- and C57BL6J mice

ABSTRACT: miR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara). Gene expression profiling (Affymetrix) was used to identify transcriptomic changes associated with psoriasis-like skin inflammation in wild type vs. miR-146a -/-mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE78057 | GEO | 2016/02/19

SECONDARY ACCESSION(S): PRJNA312479

REPOSITORIES: GEO

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Expression data from IMQ-induced psoriasis-like skin inflammation in miR-146a-/- and C57BL6J mice

Project description:miR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara). Gene expression profiling (Affymetrix) was used to identify transcriptomic changes associated with psoriasis-like skin inflammation in wild type vs. miR-146a -/-mice. A daily topical dose of 31.25 mg of Aldara cream (5% IMQ) was applied on the right ear of miR-146a -/- and C57BL/6 mice on three consecutive days to induce psorisis-like skin inflammation. Mice were sacrificed at day 4. Ear flaps were collected for total RNA extraction and hybridization on Affymatrix GeneTitan plate format Gene ST 2.1 (mouse).

2016-02-19 | E-GEOD-78057 | biostudies-arrayexpress

Microarray analysis of the brain response to cutaneous Aldara treatment

Project description:Analysis of whole mouse brain following peripheral, cutaneous immune stimulation with Aldara cream or aquaeous control cream. Results provide insight into the central response to peripheral inflammation Microarrays were used to investigate the global gene expression of mouse brains following peripheral, cutaneous application of Aldara cream or control cream C57BL/6 mice were treated with 80mg topical Aldara cream or aquaeous control cream every 24 hours for 5 consecutive days. 24 hours following the final application, brains were removed and RNA was extracted using RNeasy Mini Kit (Qiagen). 5 brains from each group were analysed using full genome Affymetrix GeneChip array

2016-08-19 | E-GEOD-72214 | biostudies-arrayexpress

Microarray analysis of the brain response to cutaneous Aldara treatment

2016-08-19 | GSE72214 | GEO

Expression data from Imiquimod-induced psoriasis mouse model

Project description:Psoriasis is a chronic inflammatory skin disorder that is predominantly characterized by sharply demarcated chronic erythematous plaques. Although its etiological mechanisms are largely unknown, recent evidence suggests that the topical application of imiquimod (IMQ) cream causes psoriasis-like skin inflammation in humans and mice. Skin examined 4 hours after IMQ cream treatment. Results provide insight into the role of each knockout mice phenotype in the response to IMQ-induced psoriasis model.

2017-10-06 | GSE104603 | GEO

FAM3C/ILEI protein is elevated in psoriatic lesions and triggers psoriasiform hyperproliferation in mice

Project description:Inducible keratinocyte-specific ILEI overexpression in mice (K5-ILEIind) recapitulates many aspects of psoriasis following TPA challenge, primarily manifested by impaired epidermal differentiation and increased neutrophil recruitment. Mechanistically, ILEI triggers Erk and Akt signaling, which then activate STAT3 via Ser727 phosphorylation. Keratinocyte-specific ILEI deletion ameliorates TPA-induced skin inflammation. A transcriptomic ILEI signature obtained from the K5-ILEIind model shows enrichment in several signaling pathways also found in psoriasis and identifies urokinase as a targetable enzyme to counteract ILEI activity. Pharmacological inhibition of urokinase in TPA-induced K5-ILEIind mice results in significant improvement of psoriasiform symptoms by reducing ILEI secretion. The ILEI signature distinguishes psoriasis from healthy skin with uPA ranking among the top “separator” genes. Our study identifies ILEI as a key driver in psoriasis, indicates the relevance of ILEI-regulated genes for disease manifestation and shows the clinical impact of ILEI and urokinase as novel potential therapeutic targets in psoriasis.

2023-04-12 | E-MTAB-12849 | biostudies-arrayexpress

Soluble adenylyl cyclase induces type 17 inflammation and is a potential therapeutic target in psoriasis

Project description:Cyclic AMP (cAMP) has a key role in psoriasis pathogenesis, as indicated by the therapeutic efficacy of phosphodiesterase inhibitors that prevent the degradation of cAMP. However, whether soluble adenylate cyclase (sAC) (encoded by the ADCY10 gene), which is an important source for cAMP, is involved in Th17 cell-mediated inflammation or could be an alternative therapeutic target in psoriasis is unknown. We have utilized the imiquimod model of murine psoriasiform dermatitis to address this question. Adcy10-/- mice had reduced erythema, scaling and swelling in the skin and Th17 cell numbers in the draining lymph nodes, compared with wild-type mice after induction of psoriasiform dermatitis with imiquimod. During Th17 polarization in vitro, naïve T cells from Adcy10-/- mice were unable to differentiate to Th17 cells and RNA-seq analysis revealed that sAC was also essential for Th17 cell activation. Interestingly, sAC did not impact Th17 lineage-defining transcription factors (such as RORc and cMAF) but rather was required for CREB-dependent gene expression. Finally, topical application of small molecule sAC inhibitors (sACi) reduced imiquimod-induced psoriasiform dermatitis and IL17 gene expression in the skin. Collectively, these findings demonstrate that sAC is a key factor for inducing type 17 inflammation in the skin and sACi could provide an alternative class of topical therapeutics for psoriasis.

2021-10-01 | GSE175470 | GEO

KLK6 expression in skin induces PAR1-mediated psoriasiform dermatitis and inflammatory joint disease

Project description:Kallikrein-related peptidase 6 (KLK6) is a secreted serine protease hypothesized to promote inflammation via cleavage of protease-activated receptors (PAR)1 and PAR2. KLK6 levels are elevated in multiple inflammatory and autoimmune conditions, but no definitive role in pathogenesis has been established. Here, we show that skin-targeted overexpression of KLK6 causes generalized, severe psoriasiform dermatitis with spontaneous development of debilitating psoriatic arthritis-like joint disease. The psoriatic skin and joint phenotypes are reversed by normalization of skin KLK6 levels and attenuated following genetic elimination of PAR1 but not PAR2. Conservation of this regulatory pathway was confirmed in human psoriasis using vorapaxar, an FDA-approved PAR1 antagonist, on explanted lesional skin from psoriasis patients. Beyond defining a critical role for KLK6-PAR1 signaling in promoting psoriasis, our results demonstrate that KLK6-PAR1-mediated inflammation in the skin alone is sufficient to drive inflammatory joint disease. Further, we identify PAR1 as a promising cytokine-independent target in therapy of psoriasis and psoriatic arthritis.

2020-03-25 | GSE144312 | GEO

IL-36 signaling in keratinocytes controls early IL-23 production in Aldara®-induced skin inflammation in mice

Project description:IL-36R signaling plays an important role in the pathogenesis of psoriasis. We ought to assess the specific function of IL-36R in keratinocytes for the pathology of Aldara®-induced psoriasis-like skin inflammation. Il36r-/- (KO) and Il36rΔK (DK) mice as well as their littermate controls, respectively Il36r+/+ (WT) and Il36rfl/fl (FL) mice, were challenged with the topical application of Aldara® on one ear during 3 or 7 days. RNASeq was performed on treated (AL) and untreated (CT) ears. Fold change analysis combined with RPKM and RT-qPCR allowed us to identify genes which were specifically regulated by IL-36R signaling in keratinocytes during the course of the treatment. We notably demonstrated that both IL-23 subunits (Il23a and Il12b) fell into this category.

2020-04-23 | GSE143688 | GEO

Mus musculus

Project description:Expression data from IMQ-induced psoriasis-like skin inflammation in miR-146a-/- and C57BL6J mice

| PRJNA312479 | ENA

A maternally inherited polymorphism in mitochondrial genome alters immune cell metabolism and protects mice from skin inflammation

Project description:Several mitochondrial genetic variants have been associated with different chronic inflammatory diseases. However, experimental proof for the pathogenic relevance of these associations is still missing. We have reported that polymorphisms in the mitochondrial gene MT-ATP8, which encodes a subunit of the mitochondrial ATP synthase, are associated with the autoimmune skin disease bullous pemphigoid. Using a mouse model for this disease, we show here that a SNP in mt-Atp8 determine the severity of autoantibody-induced skin inflammation by modulating T effector cell function and shifting the levels of short chain fatty acids. With respect to the latter, increased levels of propionate are associated with milder disease, and systemic administration of propionate ameliorates disease. By employing the Aldara™-induced psoriasiform dermatitis model, we further demonstrate that the immunomodulatory effects of mt-Atp8 variants are also relevant for autoinflammation. Collectively, our results highlight discrete mitochondrial genetic variants as significant general modulators of skin inflammation and possibly of other organs.

2020-02-13 | GSE126956 | GEO

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