Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA182384 | ENA |
REPOSITORIES: ENA
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Project description:methylation profile of dermal MSCs derived from psoriasis patients and normal control
| PRJNA182385 | ENA
Project description:mRNA expression profile of dermal MSCs derived from psoriasis patients and normal control
| PRJNA182383 | ENA
Project description:Several studies have suggested that MSCs have pleiotropic immuno-modulatory effects, including inhibition of T cell proliferation, suppression of NK cells proliferation, modulation of cytokine production, and inhibition of dendritic cell (DC) maturation etc. But the exactly mechanism are still largely unclear. We proposed to investigate the microRNA expression profile of psoriatic MSCs. 6 patients and 6 normal control were inrolled in the study, the microRNA expression profile of dermal MSCs were studied using the microarry.
2012-11-30 | E-GEOD-42633 | biostudies-arrayexpress
Project description:Several studies have suggested that MSCs have pleiotropic immuno-modulatory effects, including inhibition of T cell proliferation, suppression of NK cells proliferation, modulation of cytokine production, and inhibition of dendritic cell (DC) maturation etc. But the exactly mechanism are still largely unclear.We have found that the gene expression profile of psoriatic dermal MSCs was distinct different from normal MSCs. We proposed to investigate the DNA methylation profile of psoriatic MSCs. 6 patients and 6 normal control were inrolled in the study, the DNA methylation profile of dermal MSCs were studied using the microarry.
2012-11-30 | E-GEOD-42634 | biostudies-arrayexpress
Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion. Global gene expression profile of normal dermal lymphatic endothelial cells (ndLECs) compared to dermal lymphatic endothelial cells derived from type 2 diabetic patients (dLECs).Quadruplicate biological samples were analyzed from human lymphatic endothelial cells (4 x diabetic; 4 x non-diabetic). subsets: 1 disease state set (dLECs), 1 control set (ndLECs)
2012-06-01 | E-GEOD-38396 | biostudies-arrayexpress
Project description:Several studies have suggested that MSCs have pleiotropic immuno-modulatory effects, including inhibition of T cell proliferation, suppression of NK cells proliferation, modulation of cytokine production, and inhibition of dendritic cell (DC) maturation etc. But the exactly mechanism are still largely unclear. We proposed to investigate the mRNA expression profile of psoriatic MSCs. 6 patients and 6 normal control were inrolled in the study, the mRNA expression profile of dermal MSCs were studied using the microarry.
2012-11-30 | E-GEOD-42632 | biostudies-arrayexpress
Project description:MicroRNA expression profile of breast cancer patients with adjacent normal control group.
| PRJNA195576 | ENA
Project description:The objectives of this study were to assess differences in Bone Marrow Derived Menenchymal Stromal Cells (MSCs) during co-culture with myeloma cells, and to assess differences in myeloma patient MSCs compared to normal donor MSCs. In the study presented here, a Bone Marrow Derived Menenchymal Stromal Cells (MSCs) were analyzed after FACS sorting from 2 week culture in osteogenic media lacking dexamethasone in 3D silk scaffold matrices either in co-culture with the multiple myeloma cell line GFP+Luc+MM1.S or Alone, as controls. Also, monocultures of MSCs grown in 2D, in MSC expansion media, from Normal Donor Controls (ND) or Multiple myeloma patients (MM) were analyzed. Analysis was done looking at microRNA expression in samples with the nanoString microRNA platform for 800 microRNAs.
2014-11-01 | E-GEOD-60423 | biostudies-arrayexpress
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.
2014-12-02 | GSE63741 | 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. Epidermis samples from affected ears derived from 3 CD18hypo PL/J mice (DIS) or normal ears derived from 3 CD18hypo C57BL/6J mice(2128) were used for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare miRNA expression of normal skin from control and lesional skin.
2013-12-31 | E-GEOD-50099 | biostudies-arrayexpress