Expression data from intestinal epithelial cells (IECs)
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ABSTRACT:
PROVIDER: PRJNA247392 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of role of small intestinal epithelial cells (IECs) in the immunopathology of celiac disease
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Project description:Intestinal epithelial cells (IECs) were isolated from the colon of Villin-CreERT2, Rnf20-flox and Rnf40-flox mice two weeks upon the Tamoxifen-induced, intestinal knockout of Rnf20 and Rnf40. RNA was isolated from snap-frozen IECs to perform mRNA-seq.
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Project description:The development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3?IEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3?IEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3?IEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3?IEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis. In this study, we performed gene expression profiling to examine how the transcriptional profiles in primary live, EpCAM+ IECs from the large intestine differed between control HDAC3FF mice (3 biological replicates) and IEC-intrinsic knockout HDAC3?IEC mice (3 biological replicates).
2013-11-12 | E-GEOD-50188 | biostudies-arrayexpress
Project description:Intestinal epithelial cells (IECs) were isolated from the colon of Villin-CreERT2, Rnf20-flox and Rnf40-flox mice two weeks upon the Tamoxifen-induced, intestinal knockout of Rnf20 and Rnf40. ChIP-seq for H3K4me3 was performed using snap-frozen IECs.
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Project description:Intestinal epithelial cells were isolated from total small intestine of each four 28-day old conventionally raised (conv) and germ-free (GF) bred C57BL/6 mice (protocol according to: Lotz et al., J. Exp Med. 2006). Total RNA was isolated by TriZol and ist purity was examined using a Bioanalyszer. We used microarrays to comparatively detail the global gene expression in primary total isolated intestinal epithelial cells. Four biological replicates from isolated intestinal epithelial cells obtained from each 4 germ-free bred and conventionally raised mice. Colour change.
2012-05-16 | E-GEOD-35597 | biostudies-arrayexpress
Project description:The development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3ΔIEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3ΔIEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3ΔIEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3ΔIEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis. Analyses of histone acetylation in primary IECs from HDAC3FF (3 biologic replicates) and HDAC3ΔIEC (3 biologic replicates) mice were conducted utilizing ChIP-seq for H3K9Ac.
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Project description:Intestinal epithelial cells were isolated from total small intestine of each four 3- and 21-day-old C57BL/6 mice (protocol according to: Lotz et al., J. Exp. Med. 2006). Each two 3- and 21-day-old animals were obtained from one litter. Total RNA was isolated by TriZol and ist purity was examined using a Bioanalyszer. We used microarrays to detail the global gene expression in primary total isolated intestinal epithelial cells of 3- versus 21-day-old mice. Four biological replicates from isolated intestinal epithelial cells obtained from 3- and 21-day-old mice (each two animals from one litter). Colour change.
2012-05-16 | E-GEOD-35596 | biostudies-arrayexpress
Project description:Intestinal epithelial cells were isolated from total small intestine of each four 28-day old conventionally raised (conv) and germ-free (GF) bred C57BL/6 mice (protocol according to: Lotz et al., J. Exp Med. 2006). Total RNA was isolated by TriZol and ist purity was examined using a Bioanalyszer. We used microarrays to comparatively detail the global gene expression in primary total isolated intestinal epithelial cells.
2012-05-17 | GSE35597 | GEO
Project description:The development and severity of inflammatory bowel diseases (IBD) and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that intestinal epithelial cells (IECs) isolated from IBD patients exhibit decreased expression of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3). Further, genome-wide analyses of murine IECs that lack HDAC3 (HDAC3ΔIEC) revealed that HDAC3 deficiency resulted in dysregulated gene expression coupled with alterations in histone acetylation. Critically, conventionally-housed HDAC3ΔIEC mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3ΔIEC mice exhibited significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 plays a central role in maintaining intestinal homeostasis. Strikingly, rederivation of HDAC3ΔIEC mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis, and intestinal barrier function were largely restored in the absence of commensal bacteria. Collectively, these data indicate that the HDAC3 is a critical factor that integrates commensal bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis. In this study, we performed gene expression profiling to examine how the transcriptional profiles in primary live, EpCAM+ IECs from the large intestine differed between germ-free control HDAC3FF mice (3 biological replicates) and germ-free IEC-intrinsic knockout HDAC3ΔIEC mice (3 biological replicates).
2013-11-12 | E-GEOD-50189 | biostudies-arrayexpress
Project description:We profiled genome-wide accesssible chromatin data and RNA-seq from four species (zebrafish, stickleback, mouse, and human) to identify commonly regulated genes and regulatory metods in intestinal epithelial cells (IECs). We identify a group genes that are commonly expressed in IECs and genes that are commonly expressed along the length of the intestine in fish and mammals. Using accessible chromatin data we identified enriched transcription factor binding site motifs In IECs and sites that are commonly accessible in IECs in all species. Finally, we confirm the ability for these regions from multiple species to drive conserved expression in IECs using a zebrafish reporter assay.
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