Ontology highlight
ABSTRACT:
PROVIDER: PRJNA908222 | ENA |
REPOSITORIES: ENA
Similar Datasets
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 | PXD025770 | Pride
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
Project description:In order to unravel the impact of intestinal smooth muscle tissue on the intestinal epithelium, we isolated clean smooth muscle, cultured it for 24h in DMEM-F12, and collected the supernatant (muscle-SN). This supernatant was used to treat small intestinal organoids (made of intestinal epithelium), compared to normal ENR treatment. After 5 days of muscle-SN exposure, we disrupted the organoids, and directly isolate the RNA. RNA-seq was performed in this sample to assess the genetic changes induced by muscle products.
2021-09-27 | E-MTAB-9181 | biostudies-arrayexpress
Project description:The etiology of post-inflammatory gastrointestinal (GI) motility dysfunction, after resolution of acute symptoms of inflammatory bowel diseases (IBD) and intestinal infection, is largely unknown. Here, using an established mouse model of experimental enteritis, we show that enhancement of smooth muscle cell (SMC) contraction by interleukin (IL)-17A may be involved in postinflammatory GI hypermotility. To examine the effect of IL-17 in the small intestinal smooth muscle, we used whole genome microarray expression profiling to find out the genes which respond to IL-17 stimulus. The smooth muscle strips were peeled off from mouse small intestine and incubated 24h with or without IL-17. And we also examined the effect of 6-shogaol, which is one of the ingredients of Japanese traditional medicine for intestinal mortor disorder, Daikenchuto, in IL-17 stimulated small intestinal smooth muscle strip. The smooth muscle strips were peeled off from mice small intestine and incubated in the culture media for 24h with or without IL-17. A part of IL-17 stimulated strips were co-incubated with 6-shogaol. Six independent experiments were performed.
2012-09-15 | E-GEOD-39573 | biostudies-arrayexpress
Project description:To identify novel genes especially lncRNAs linked to vascular smooth muscle cell (VSMC) differentiation, we performed RNA sequencing of adenovirus–MYOCD transduced human coronary artery smooth muscle cells (HCASMs). Simiilar amount of empty Adenovirus was used as control.
2016-08-31 | GSE77120 | GEO
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:We report a novel technique to reprogram human fibroblasts into endothelial and smooth muscle cells using partial iPSC reprogramming and chemically defined media. Using appropriate media conditions for differentiation of human pluripotent cells to CD34+ vascular progenitor cells, we show that temporary expression of pluripotent transcription factors and treatment with chemically-defined media, will induce differentiation of human fibroblasts to CD34+ vascular progenitor cells. Sorted CD34+ cells can then be directed to differentiate into vascular endothelial cells expressing a variety of smooth muscle markers. We have assessed the global DNA methylation (Illumina Infinium HD 450K DNA methylationBeadChips) and transcriptional (Illumina HT12v4 Gene Expression Bead Array) profiles of transdifferentiated endothelial cells and smooth muscle, human embryonic stem cell (hESC) and human induced pluripotent stem cell (hiPSC) differentiated CD34+ angioblasts, hESCs, hiPSC, primary smooth muscle and primary human umbilical vein endothelial cells using microarrays.
2012-09-18 | E-GEOD-40909 | biostudies-arrayexpress
Project description:We report a novel technique to reprogram human fibroblasts into endothelial and smooth muscle cells using partial iPSC reprogramming and chemically defined media. Using appropriate media conditions for differentiation of human pluripotent cells to CD34+ vascular progenitor cells, we show that temporary expression of pluripotent transcription factors and treatment with chemically-defined media, will induce differentiation of human fibroblasts to CD34+ vascular progenitor cells. Sorted CD34+ cells can then be directed to differentiate into vascular endothelial cells expressing a variety of smooth muscle markers. We have assessed the global DNA methylation (Illumina Infinium HD 450K DNA methylationBeadChips) and transcriptional (Illumina HT12v3 and HT12v4 Gene Expression Bead Array) profiles of transdifferentiated endothelial cells and smooth muscle, human embryonic stem cell (hESC) and human induced pluripotent stem cell (hiPSC) differentiated CD34+ angioblasts, hESCs, hiPSC, primary smooth muscle and primary human umbilical vein endothelial cells using microarrays.
2012-09-18 | E-GEOD-40793 | biostudies-arrayexpress
Project description:The etiology of post-inflammatory gastrointestinal (GI) motility dysfunction, after resolution of acute symptoms of inflammatory bowel diseases (IBD) and intestinal infection, is largely unknown. Here, using an established mouse model of experimental enteritis, we show that enhancement of smooth muscle cell (SMC) contraction by interleukin (IL)-17A may be involved in postinflammatory GI hypermotility. To examine the effect of IL-17 in the small intestinal smooth muscle, we used whole genome microarray expression profiling to find out the genes which respond to IL-17 stimulus. The smooth muscle strips were peeled off from mouse small intestine and incubated 24h with or without IL-17. And we also examined the effect of 6-shogaol, which is one of the ingredients of Japanese traditional medicine for intestinal mortor disorder, Daikenchuto, in IL-17 stimulated small intestinal smooth muscle strip.
2012-09-15 | GSE39573 | GEO