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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling by array of mouse Paneth cells from Atg16l1 mutant and wild type strains

ABSTRACT: Transcription profiling of Paneth cells from Atg16l1hm mice with CR6 virus. Normalized data is provided as an additional file on the FTP site for this experiment.

ORGANISM(S): Mus musculus

SUBMITTER: Chad Storer

PROVIDER: E-TABM-958 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of Paneth cells from Atg16l1hm mice with CR6 virus

Project description:Transcription profiling of Paneth cells from Atg16l1hm mice with CR6 virus

2010-04-09 | E-TABM-957 | biostudies-arrayexpress

Transcription profiling of DBA/1J mouse with collagen induced arthritis

Project description:Time course of collagen-induced arthritis in DBA/1J male mice, synchronized on day 28 with 10ug LPS

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Transcription profiling by array of mouse hind paws after receiving KRN T cells from K/BxN mice

Project description:K/BxN mice were generated by crossing KRN males with NOD females, and it was these mice that served as the source for the T cells adoptively transferred. Male B6.TCR.Ca-/-H-2b/g7 (recipient) mice age 10-14 weeks old were used in this model and are the source of the paw tissue profiled in this study.

2010-04-23 | E-TABM-966 | biostudies-arrayexpress

Microarray of laser capture microdissected Paneth cells from Atg16l1 T300A and wildtype littermates mice that were either exposed or not with mainstream cigarette smoking for 6 weeks

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed transcriptional profiling to identify molecular mechanisms associated with Paneth cell defect in Atg16l1 T300A mice exposed to cigarette smoking. Female mice were used at 4-5 weeks of age. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. The Paneth cells of the mice were harvested by laser capture microdissection for transcriptomic analysis after completing 6 weeks of smoking.

2018-10-31 | E-MTAB-6168 | biostudies-arrayexpress

Expression data from Paneth cells isolated from mice on calorie restricted or ad libitum diet

Project description:Paneth cells recide in the intestinal crypt bottom and are part of the innate immunity and of the intestinal stem cell niche. We used microarrays to detail the global changes in gene expression following reduced calorie intake. Mice were kept on ad libitum or calorie restricted (60% of calories of ad libitum) diets for 4-7 weeks and paneth cells were isolated using flowcytometry

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Paneth cells constitute the niche for Lgr5 stem cells in intestinal crypts

Project description:Homeostasis of self-renewing small intestinal crypts results from neutral competition between Lgr5 stem cells, small cycling cells located at crypt bottoms1, 2. Lgr5 stem cells are interspersed between terminally differentiated Paneth cells, that are known to produce bactericidal products such as lysozyme and cryptdins/defensins3. Single Lgr5-expressing stem cells can be cultured to form long-lived, self-organizing crypt-villus organoids in the absence of non-epithelial niche cells4. Here, we note a close physical association of Lgr5 stem cells with Paneth cells in vivo and in vitro. CD24+ Paneth cells express EGF, TGF?, Wnt3 and the Notch-ligand Dll4, all essential signals for stem cell maintenance in culture. Co-culturing of sorted stem cells with Paneth cells dramatically improves organoid formation. This Paneth cell requirement can be substituted by a pulse of exogenous Wnt. Genetic removal of Paneth cells in vivo results in the concomitant loss of Lgr5 stem cells. In colon crypts, CD24+ cells residing between Lgr5 stem cells may represent the Paneth cell equivalents. We conclude that Lgr5 stem cells compete for essential niche signals provided by a specialized daughter cell, the Paneth cell. We used intestinal cell fractions from Lgr5-EGFP-ires-CreERT2 mice, expressing GFP under the control of the Lgr5 promoter. RNA was isolated from two FACS sorted cell populations: stem cells were sorted based on high level of GFP expression (GFPhi) and Paneth cells were sorted based on high level of CD24 expression (CD24hi) and high side-scatter (SSChi). Differentially labelled cRNA from GFPhi and CD24hi/SSChi cells from two different sorts (each combining ten individual mice) were hybridized on 4X44K Agilent Whole Mouse Genome dual colour Microarrays (G4122F) in two dye swap experiments, resulting in four individual arrays.

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RNA-seq of mouse ileum to investigate the role of IL-17 receptor signaling in Paneth cells in their biology and intestinal physiology

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Transcription profiling by array of Paneth cells and whole ileum from human Crohn's disease patient ileo-colic resection tissue

Project description:Transcriptional profiling of microscopically laser dissected Paneth cells and whole thickness ileum tissue from the proximal margins of archived formalin-fixed, paraffin-embedded ileo-colic resection samples.

2014-01-03 | E-MTAB-1281 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.

2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were either exposed or not to mainstream cigarette smoking for 6 weeks

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