Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

ABSTRACT: To find which signaling is activated in chronic inflammation, we tried to induce chronic skin and pancreas inflammation compared to normal skin and pancreas.

ORGANISM(S): Mus musculus

PROVIDER: GSE207956 | GEO | 2024/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

Project description:Skin & Pancreas chronic inflammation versus Normal Skin & Pancreas

| PRJNA857740 | ENA

Skin inflammation

Project description:IL-12 protects from psoriasiform skin inflammation

| PRJEB15422 | ENA

Inflammation-Driven Carcinogenesis is Mediated through STING [skin]

Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from DMBA or acetone treated wild type (WT) or STING deficient (SKO) mouse skin or skin tumor was examined for gene expression.

2014-05-31 | E-GEOD-57604 | biostudies-arrayexpress

Inflammation and tumor susceptibility in skin cancer

Project description:This SuperSeries is composed of the following subset Series: GSE12248: Genetic architecture of murine skin inflammation and tumor susceptibility GSE21247: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (carcinomas) GSE21263: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (papillomas) GSE26273: Network Analysis of Skin Tumor Progression Identifies a Rewired Genetic Architecture Affecting Inflammation and Tumor Susceptibility (aCGH) Refer to individual Series

2010-12-22 | E-GEOD-21264 | biostudies-arrayexpress

Localized skin inflammation during cutaneous leishmaniasis drives a chronic, systemic IFN-g signature

Project description:Localized skin inflammation during cutaneous leishmaniasis drives a chronic, systemic IFN-g signature

| PRJNA682985 | ENA

Angiogenesis in the skin of SHARPIN-deficient mice with chronic proliferative dermatitis

Project description:Angiogenesis is a common feature of pathological processes including wound healing, tumor formation, and chronic inflammation. Chronic inflammation can also be associated with dilation or proliferation of lymph vessels. We examined blood vessels and lymphatics and the expression of pro- and anti-angiogenic genes in the skin of SHARPIN-deficient mice which spontaneously develop a chronic proliferative dermatitis (cpdm). The number of blood vessels in the dermis of cpdm mice increased with age as the inflammation progressed. Lymphatics identified by labeling for LYVE1 and podoplanin were moderately dilated, but they were not increased in number. The expression of proangiogenic Vegfa, Flt1 and anti-angiogenic Sema3a mRNA was increased. VEGFA was primarily localized in keratinocytes of cpdm skin. There was also increased expression of Ece1 and Pdpn mRNA. Podoplanin was restricted to lymphatic endothelial cells in normal skin, but fibroblasts in cpdm skin also reacted with anti-podoplanin antibodies indicating that they were activated. The expression of other angiogenic and lymphangiogenic factors was not altered or decreased. These results indicate that cpdm mice may be a useful model to study the pathogenesis of angiogenesis in chronic inflammation.

2016-05-21 | GSE81683 | GEO

Der f/SEB-induced skin inflammation

Project description:Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease. We recently described an animal model in which repeated epicutaneous applications of a house dust mite extract and Staphylococcal enterotoxin B induced eczematous skin lesions. In this study we showed that global gene expression patterns are very similar between human AD skin and allergen/staphylococcal enterotoxin B–induced mouse skin lesions, particularly in the expression of genes related to epidermal growth/differentiation, skin barrier, lipid/energy metabolism, immune response, or extracellular matrix. In this model, mast cells and T cells, but not B cells or eosinophils, were shown to be required for the full expression of dermatitis, as revealed by reduced skin inflammation and reduced serum IgE levels in mice lacking mast cells or T cells (TCRb-/- or Rag1-/-). The clinical severity of dermatitis correlated with the numbers of mast cells, but not eosinophils. Consistent with the idea that T helper type 2 (Th2) cells play a predominant role in allergic diseases, the receptor for the Th2-promoting cytokine thymic stromal lymphopoietin and the high-affinity IgE receptor, FceRI, were required to attain maximal clinical scores. Therefore, this clinically relevant model provides mechanistic insights into the pathogenic mechanism of human AD. A total of six samples were analyzed. Back skin samples from healthy or AD-induced C57BL/6, PLC-beta 3 KO (C57BL/6 background), and NC/Nga mice were collected for total RNA extraction. Pooled RNA from 2-4 mice per condition were used for analysis.

2013-12-10 | E-GEOD-53132 | biostudies-arrayexpress

Profiling of Kallikrein Proteases and Global Proteome Biology of PDAC, Chronic Pancreatitis and Normal Pancreas

Project description:Cell conditioned medium from human pancreatic cancer cell lines MiaPaCa-2, AsPC-1, primary pancreatic cell lines as well as human FFPE tissue samples from pancreatic ductal adenocarcinoma (PDAC), chronic pancreatitis (CP), ampullary cancer, non-malignant adjacent pancreas and normal pancreas were analyzed via targeted (SRM, PRM) and/or explorative (DIA) mass spectrometry.

| MSV000090255 | MassIVE

MicroRNA profiling of human pancreas to identify expression patterns to differentiate pancreatic adenocarcinoma from normal pancreas and chronic pancreatitis

Project description:MicroRNA Expression Patterns to Differentiate Pancreatic Adenocarcinoma From Normal Pancreas and Chronic Pancreatitis

2010-03-11 | E-TABM-664 | biostudies-arrayexpress

Immunity to commensal skin fungi promotes psoriasiform skin inflammation

Project description:Immunity to commensal skin fungi promotes psoriasiform skin inflammation

| PRJNA605153 | ENA