Project description:Oxidative damage contributes significantly to the pathogenesis of psoriasis. We recently developed antioxidative peptides (UPF peptides) activating the endogenous glutathione system (GSH). In the present study, we analyzed gene expression profiles in the samples of psoriasis patients to find if these peptides could reduce oxidative damage during psoriasis. Peripheral blood mononuclear cells (PBMCs) from patients with psoriasis and from healthy controls were collected and cultivated. Cultured PBMCs were incubated with two different UPF peptides for 12 hours. Gene expression analysis was performed with Affymetrix Human Gene 1.0 ST arrays and with quantitative real-time PCR. Gene expression profile in the PBMCs of patients with psoriasis indicated significant up-regulation of the immune response pathway. Treatment with UPF peptides normalized the gene expression pattern in psoriasis samples. Therefore, treatment with antioxidative drugs have potential anti-psoriatic activity. 5 healthy controls (C1-5), 5 psoriasis patients (P1-5), 2 different drugs (upf17 peptide, upf1 peptide) and a control drug. Overall, 30 samples and six groups: PSOR, PSORUPF1, PSORUPF17, CON, CONUPF1, CONUPF17.
Project description:Oxidative damage contributes significantly to the pathogenesis of psoriasis. We recently developed antioxidative peptides (UPF peptides) activating the endogenous glutathione system (GSH). In the present study, we analyzed gene expression profiles in the samples of psoriasis patients to find if these peptides could reduce oxidative damage during psoriasis. Peripheral blood mononuclear cells (PBMCs) from patients with psoriasis and from healthy controls were collected and cultivated. Cultured PBMCs were incubated with two different UPF peptides for 12 hours. Gene expression analysis was performed with Affymetrix Human Gene 1.0 ST arrays and with quantitative real-time PCR. Gene expression profile in the PBMCs of patients with psoriasis indicated significant up-regulation of the immune response pathway. Treatment with UPF peptides normalized the gene expression pattern in psoriasis samples. Therefore, treatment with antioxidative drugs have potential anti-psoriatic activity.
Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
Project description:SPO11-promoted DNA double-strand breaks (DSBs) formation is a crucial step for meiotic recombination, and it is indispensable to detect the broken DNA ends accurately for dissecting the molecular mechanisms behind. Here, we report a novel technique, named DEtail-seq (DNA End tailing followed by sequencing), that can directly and quantitatively capture the meiotic DSB 3’ overhang hotspots at single-nucleotide resolution.
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.