RNA-seq of intestinal crypts vs intestinal smooth muscle with a specific MMP17 deletion compared to wild-type
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ABSTRACT:
PROVIDER: PRJEB38672 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4192570_1.fastq.gz | Fastqsanger.gz | |||
| ERR4192570_2.fastq.gz | Fastqsanger.gz | |||
| ERR4192571_1.fastq.gz | Fastqsanger.gz | |||
| ERR4192571_2.fastq.gz | Fastqsanger.gz | |||
| ERR4192572_1.fastq.gz | Fastqsanger.gz |
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Project description:We wanted to assess the role of a specific smooth muscle protein (MMP17) in two different intestinal compartments, the epithelium (crypts) and the smooth muscle. To do that we isolate intestinal crypts from wild-type (WT) and knockout (KO, Mmp17-/-) mice, and obtained clean strips of smooth muscle. After muscle dissociation, we obtained RNA directly from crypts and muscle, and it was used for RNA-seq. By comparing WT and KO samples we observed a higher impact in gene expression affecting crypts, even though MMP17 is only expressed in muscle. This helped us to identify altered signaling pathways in KO crypts that linked MMP17 with SMAD4 and BMP signaling.
2021-09-27 | E-MTAB-9180 | biostudies-arrayexpress
Project description:RNA-seq of intestinal crypts vs intestinal smooth muscle with a specific MMP17 deletion compared to wild-type
2021-03-22 | E-MTAB-9180 | ExpressionAtlas
Project description:The effort to better understand intestinal stem cell (ISC) identity and regulation remains a challenge. We have been studying the RNA-binding protein MEX3A as a putative ISC marker. In that context, we have generated the first Mex3a knockout (KO) mouse model and show MEX3A is crucial for maintenance of the Lgr5+ ISC pool. As part of a phenotypic characterization pipeline, we have performed transcriptomic profiling (RNA-sequencing) of isolated Mex3a KO small intestinal crypts and compared it against small intestinal crypts isolated from age-matched wild-type controls.
2020-02-13 | GSE141191 | GEO
Project description:To assess the role of LSD1 in mouse small intestinal epithelium, we isolated small intestinal crypts from wild type (WT) (Villin-Cre -; Lsd1f/f) and intestinal-epithelial-specific knock-out (KO) (Villin-Cre+; Lsd1f/f) mice. We dissociated crypts into single cells, and FACS sorted Epcam+ cells, to avoid immune-cell contamination. RNA was directly isolated from these sorted cells, and this was used for RNA seq. As KO crypts are different from WT crypts (KO crypts lack Paneth cells), identifying genes specifically regulated by LSD1 helps us to identify how LSD1 regulates intestinal crypt biology. Specifically, because we were able to combine this with ChIP-seq of the same cells, to identify where H3K4me1 levels (target of the histone demethylase LSD1) were different in the genome.
2020-11-16 | E-MTAB-7862 | biostudies-arrayexpress
Project description:The Wnt signaling pathway is deregulated in over 90% of human colorectal cancers. β Catenin, the central signal transducer of the Wnt pathway, can directly modulate gene expression by interacting with transcription factors of the TCF/LEF-family. In the present study we investigate the role of Wnt signaling in the homeostasis of intestinal epithelium using tissue-specific, inducible beta-catenin gene ablation in adult mice. Block of Wnt/beta-catenin signaling resulted in rapid loss of transient-amplifying cells and crypt structures. Importantly, intestinal stem cells were induced to terminally differentiate upon deletion of beta-catenin resulting in a complete block of intestinal homeostasis and fatal loss of intestinal function. Transcriptional profiling of mutant crypt mRNA isolated by laser capture micro dissection confirmed those observations and allowed to identify genes potentially responsible for the functional preservation of intestinal stem cells. Experiment Overall Design: laser capture microdissection of intestinal crypts, control vs. beta-catenin mutant (2days after induction of deletion by tamoxifen), two rounds of amplification of mRNA
2008-06-16 | E-GEOD-8818 | biostudies-arrayexpress
Project description:Transcriptomic profiling of small intestinal crypts upon MEX3A deletion
| PRJNA592553 | ENA
Project description:Our goal was to compare the transcriptomic profile of lgr5+ high, medium and low cells (corresponding to centre, border and >3 row in crypts) between small and large intestine in mice. We observed differences in the transcriptional profile between centre and border Lgr5+ cells within small and large intestinal crypts and more profound differences between the two intestinal sites.
2022-04-20 | GSE194250 | GEO
Project description:Purpose: The activation of TLR4 was reported to effectively alleviate intestinal injury induced by irradiation (IR). The goals of this study are to investigate the transcriptome profiling (RNA-seq) of intestinal crypts thereby clarifying the underlying mechanism mediating the radio-protective activity of TLR4 on intestinal stem cells. Methods: Intestinal crypts mRNA profiles of mice treated or untreated with TLR4 low-toxic agonist monophosphyal lipid A (MPLA) upon abdominal body irradiation (AIR) exposure were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500 sequencer. To pre-treated the data, adaptor and low-grade reads removal, low-quality bases elimination from 3' or 5' ends, original and effective sequencing quantity analysis, as well as guanine and cytosine statistics were subjected, in turns. Differential expression genes were selected via correlation test, principal component analysis and cluster analysis, in which the fold change (FC) was greater than 2 and p value was less than 0.05 could be regarded significance. Different expressed genes (DEGs) were clustered into pathways of intestinal crypts through KEGG. Results: As compared to the nonirradiated group, 2733 DEGs were identified in intestinal crypts after AIR damage, while there were 2168 DEGs between irradiated group and irradiated plus MPLA treatment group. Among the DEGs, a series of genes involving intestinal stem cells regeneration, which mainly falls into three stem cell related pathway according to Gene ontology analysis and KEGG enrichment: Hippo, Wnt and Notch signaling pathway. Based on these DEGs, we focused on a group of genes which was suppressed by IR, while could be restored by TLR4 activation. Based on the criteria, 8 DEGs (SOX9, cMyc, MSI1, Lgr5, Notch1, Wnt5b, Axin2, DLL4) involving intestinal stem cell regulation were further selected for validation, from which the mRNA levels of 4 genes (SOX9, YAP1, cMyc) were confirmed to be up-regulated by MPLA treatment. Conclusions: Our study represents the first detailed analysis of intestinal crypts transcriptomes by TLR4 activation upon IR damage, with biologic replicates, generated by RNA-seq technology. And the confirmation of DEGs will facilitate the development of novel targets and techniques to efficiently stimulate the regeneration of intestinal stem cells to reconstruct the intestine after radiation injury.
2025-03-01 | GSE197682 | GEO
Project description:Polycomb-mediated gene repression plays an important role in adult stem cell maintenance. Direct targets of the Polycomb repressive complex PRC2 in th intestinal epithelium were revealed by performing ChIP-sequencing on crypt samples isolated from wild type murine small intestines. The resulting list of H3K27me3-enriched genes were compared with RNA-sequencing data from wild type and Eed knockout crypts. Crypts were isolated from wild type murine intestinal epithelium and subjected to ChIP using anti-H3K27me3 and anti-H3K27Ac antibodies, after which DNA isolated from extracted immunocomplexes was sequenced.
2016-07-01 | E-GEOD-81577 | biostudies-arrayexpress
Project description:Smooth muscle is an essential component of the intestine, both to maintain its structure and produce peristaltic and segmentation movements. However, very little is known about other putative roles that smooth muscle may have. Here, we show that smooth muscle is the dominant supplier of BMP antagonists, which are niche factors that are essential for intestinal stem cell maintenance. Furthermore, muscle-derived factors can render epithelium reparative and fetal-like, which includes heightened YAP activity. Mechanistically, we find that the matrix metalloproteinase MMP17, which is exclusively expressed by smooth muscle, is required for intestinal epithelial repair after inflammation- or irradiation-induced injury. Furthermore, we provide evidence that MMP17 affects intestinal epithelial reprogramming indirectly by cleaving the matricellular protein PERIOSTIN, which itself is able to activate YAP. Together, we identify an important signaling axis that firmly establishes a role for smooth muscle as a modulator of intestinal epithelial regeneration and the intestinal stem cell niche.
2021-11-02 | PXD020561 | Pride