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Gene expression profile of goblet cells (GCs) from the distal colon (DC) and the 8th portion of the small intestine (Si8)

ABSTRACT: Gene expression profile of goblet cells (GCs) from the distal colon (DC) and the 8th portion of the small intestine (Si8)

PROVIDER: PRJNA603500 | ENA |

REPOSITORIES: ENA

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Gene expression profile of goblet cells (GCs) from the distal colon (DC) and the 8th portion of the small intestine (Si8)

Project description:Goblet cells together other cell types make up the intestinal epithelium and are responsible for mucus production. The goal of this project is to fully characterize the gene expression profile of the GCs in the colon and small intestine.

2021-04-16 | GSE144363 | GEO

Gene expression profile at single cell level of goblet cells (GCs) from the distal colon (DC) and the 8th portion of the small intestine (Si8)

Project description:Goblet cells are considered as a homogeneous population in the intestinal epithelium. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of GCs in the intestine.

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Gene expression profile at single cell level of goblet cells (GCs) from the distal colon (DC) and the 8th portion of the small intestine (Si8)

Project description:Gene expression profile at single cell level of goblet cells (GCs) from the distal colon (DC) and the 8th portion of the small intestine (Si8)

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Gene expression profile at single cell level of goblet cells (GCs) from the distal colon (DC) and the 8th portion of the small intestine (Si8)

Project description:Objective: Benign prostatic hyperplasia (BPH) is a common disease in men over 50 years old, which seriously reduces the quality of life of patients. At present, the transcriptome changes of gene expression profile in benign prostatic hyperplasia have not been explored to a great extent. Methods: In this study, single-cell RNA sequencing was performed on the isolated prostate tissue of BPH mice, and its cell types were identified and enriched. In addition, we constructed the cell communication network and sequence analysis, revealing its receptor-ligand pair and its transmission signals with other cells. Results: The results revealed the changes in 11 cell subpopulations including B cells, DC, Endothelial cells, Epithelial cells, Fibroblast & Myofibroblast, Macrophage, Mast cells, Satellite cells, Schwann cells, Smooth Muscle cells, and T Cell & NK & NKT in the microenvironment at various stages of the occurrence and development of benign prostatic hyperplasia, and updated the understanding of Epithelial cells, Fibroblast & Myofibroblast cell markers. Conclusion: Our study promotes the understanding of cellular dynamic changes and potential molecular mechanisms in the development of BPH.

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Gene expression profile of colonic goblet cells (GCs) from SpdefKO_RedMUC298trTg and RedMUC298trTg mice

Project description:Gene expression profile of colonic goblet cells (GCs) from SpdefKO_RedMUC298trTg and RedMUC298trTg mice

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Gene expression profile of colonic goblet cells (GCs) from SpdefKO_RedMUC298trTg and RedMUC298trTg mice

Project description:Spdef is a transcription factor involved in differentiation of goblet cells. Goblet cells from RedMUC298trTg and Spdef -/-RedMUC298trTg were sorted to analyse the differential gene expression in the absence of Spdef.

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Transcription profiling of mouse allergen-induced goblet cells

Project description:High numbers of goblet cells in airways contribute to the mucus obstruction characteristic of asthmatic airways. Allergen challenged mice exhibit robust expression of goblet cells within airway surface epithelium. This study looks at the temporal analysis of IL-13 exposed murine airways to elucidate pathways that result in differentiation of airway epithelial cells to goblet cells.

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Allergen-induced goblet cells

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Armatimonadetes bacterium DC isolate:DC

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Effects of HSP90 inhibitors on airway goblet cell metaplasia

Project description:Goblet cell metaplasia and mucus hypersecretion are disabling hallmarks of chronic lung diseases for which no curative treatments are available. Therapies targeting specific upstream drivers of asthma have had variable results. We hypothesized that an a priori-knowledge independent approach would point to new therapies for airway goblet cell metaplasia. We analyzed the transcriptome of an organotypic model of human goblet cell metaplasia. We combined our data with previously published datasets from IL13-exposed in vitro and asthmatic in vivo human airway epithelial cells. The drug perturbation-response connectivity approach identified the heat shock protein 90 (HSP90) inhibitor geldanamycin as a candidate for reverting airway goblet cell metaplasia. We found that geldanamycin not only prevented but reverted IL13-induced goblet cell metaplasia. Geldanamycin did not induce goblet cell death, did not solely block mucin synthesis, and did not block IL13 receptor-proximal signaling. Moreover, the transcriptional effects of geldanamycin were absent in unstimulated cells and became evident only after stimulation with IL13. The predicted mechanism of action suggested that geldanamycin should also revert IL17-induced goblet cell metaplasia, a prediction confirmed by our data. Our findings suggest HSP90 activity may be required for persistence of goblet cell metaplasia driven by various mechanisms in chronic lung diseases.

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