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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse colon from wild-type and Slc9a3 (NHE3)-deficient animals

ABSTRACT: Na+/H+ exchanger 3 (NHE3) provides a major route for intestinal Na+ absorption. It has been considered as a target of proinflammatory cytokines and enteropathogenic bacteria and impaired NHE3 expression and/or activity may be responsible for inflammation-associated diarrhea. We used microarray analysis to detail the global programme of colonic gene expression in the absence of functional NHE3. Experiment Overall Design: Whole colon was dissected from 6-8 week old NHE3-deficient mice and their wild-type littermates and total RNA isolated for microarray analysis using Affymetrix murine MOE430 2.0 arrays

ORGANISM(S): Mus musculus

SUBMITTER: Pawel Kiela

PROVIDER: E-GEOD-10740 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from the colon of wild-type and Slc9a3 (NHE3)-deficient mice

Project description:Na+/H+ exchanger 3 (NHE3) provides a major route for intestinal Na+ absorption. It has been considered as a target of proinflammatory cytokines and enteropathogenic bacteria and impaired NHE3 expression and/or activity may be responsible for inflammation-associated diarrhea. We used microarray analysis to detail the global programme of colonic gene expression in the absence of functional NHE3. Keywords: knockout effect

2008-03-06 | GSE10740 | GEO

Coordinated assembly of NHE3, IRBIT, NHERF1, and ezrin ameliorates fluid malabsorption in diabetes

Project description:Clinical evidence supports the occurrence of intermittent diarrhea in many type 1 diabetes mellitus (T1DM) patients. Others and we found that net fluid absorption rate is dramatically lower in the ileum of T1DM murine models. However, the identity of molecules that contribute to fluid malabsorption in the gut remains unknown. Considering the importance of ion transporters and channels for intestinal fluid absorption, we reasoned that their expression level at the luminal membrane is altered under diabetic conditions. To this end, we analyzed the brush border membrane vesicles (BBMVs) from the ileum of control and DM mice by proteomic analysis. The expression levels of Cl-/HCO3- exchanger SLC26A3/DRA and cystic fibrosis transmembrane conductance regulator (CFTR) were not significantly different between control and DM mice. Cl-/HCO3- exchanger Slc26a6/PAT1 and Na+/H+ exchanger 3 (NHE3) were not detected. Interestingly, cytoskeleton scaffold proteins that regulate NHE3, including NHERF1-3 and ezrin, were all significantly lower in diabetic animals.

2016-04-27 | PXD001859 | Pride

The effects of dietary curcumin on colonic gene expression in TNBS-induced colitis

Project description:Curcumin is a potent anti-inflammatory compound capable of preventing chemically induced colitis in mice. We used microarray analysis to detail the global programme of colonic gene expression in BALB/c mice fed standard or 2% curcumin-supplemented diet and treated with control or TNBS (trnitrobenzene-sulfonic acid, 2 mg/mouse) enema. Keywords: Diet and disease effect. 6-8 week old BALB/c mice were treated with respective diet two days prior to enema administration (day 0) and sacrificed on day 7. Whole colon was dissected from mice and their wild-type littermates and total RNA isolated for microarray analysis using Affymetrix murine MOE430 mouse array set. RNA was pooled from 3 mice in each dietary/treatment group.

2008-11-21 | E-GEOD-13705 | biostudies-arrayexpress

Disruption of Na+/H+ exchanger regulatory factor 2 scaffold suppresses colon cancer proliferation

Project description:A key function of Na+/H+ exchanger regulatory factor 2 (NHERF2) is spatial organization of signaling proteins to facilitate signal transduction. The role of NHERF2 in cancer progress is not well understood. This study determines how loss of NHERF2 alter colon cancer progress.

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NCX1 represents an ionic Na+ sensing mechanism in macrophages

Project description:Inflammation and infection can trigger local tissue Na+-accumulation. This Na+-rich environment boosts pro-inflammatory activation of monocyte/macrophage-like cells (MΦ) and their antimicrobial activity. Enhanced Na+-driven MΦ-function requires the osmoprotective transcription factor nuclear factor of activated T cells 5 (NFAT5), which augments NO production and contributes to increased autophagy. However, the mechanism of Na+-sensing in MΦ remained unclear. High extracellular Na+ levels (HS) trigger a substantial Na+-influx and Ca2+ loss. Here, we show that the Na+/ Ca2+-exchanger 1 (NCX1/ solute carrier family 8 member A1 (SLC8A1)) plays a critical role in HS-triggered Na+-influx, concomitant Ca2+ efflux and subsequent NFAT5 accumulation. Moreover, interfering with NCX1-activity impairs HS-boosted inflammatory signaling, infection-triggered autolysosome formation and subsequent antibacterial activity. Taken together, this demonstrates that NCX1 is able to sense Na+ and is required for amplifying inflammatory and antimicrobial MΦ responses upon HS exposure. Manipulating NCX1 offers a new strategy to regulate MΦ function.

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Influence of G. lamblia infection on the transcriptional profile in intestinal and liver tissue [liver]

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Influence of G. lamblia infection on the transcriptional profile in intestinal and liver tissue [intestinal epithelial cells]

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Project description:G. lamblia is a fecal-oral transmitted human enteropathogenic protozoan with extremely high incidence in endemic areas in Africa and Asia particularly in the infant population. It homes to the proximal small intestine and induceses diarrhea and malabsoption. Here we established a novel murine G. lamblia infection model and analyzed the tissue and epithelial response and downstream microbial and metabolic effects in the adult host.

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Project description:G. lamblia is a fecal-oral transmitted human enteropathogenic protozoan with extremely high incidence in endemic areas in Africa and Asia particularly in the infant population. It homes to the proximal small intestine and induceses diarrhea and malabsoption. Here we established a novel murine G. lamblia infection model and analyzed the tissue and epithelial response and downstream microbial and metabolic effects in the adult host.

2020-04-03 | GSE148081 | GEO

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