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RNA-Seq of distal colonic homogenates from intestinal epithelial-specific Sprouty2-deleted mice versus littermate controls

ABSTRACT: We asked whether Sprouty2 controls secretory cell differentiation in the distal colon. Loss of Sprouty2 leads to expansion of tuft and goblet cell populations. Sprouty2 loss induced PI3K/Akt signaling, leading to GSK3β inhibition and epithelial IL-33 expression

ORGANISM(S): Mus musculus

PROVIDER: GSE160854 | GEO | 2020/11/14

REPOSITORIES: GEO

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Single cell RNA seq of colonic tissue from intestinal epithelial-specific Sprouty2-deleted mice and controls

Project description:In this study we asked how loss of Sprouty2 remodels colonic tissue and function. We show that loss of Sprouty2 promotes IL-13 signaling to regulate colonic secretory cells and furthermore identify deep crypt secretory cells as a reservoir for the host defense peptide RELMbeta.

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RNA-Seq of distal colonic homogenates from intestinal epithelial-specific Sprouty2-deleted mice versus littermate controls

Project description:RNA-Seq of distal colonic homogenates from intestinal epithelial-specific Sprouty2-deleted mice versus littermate controls

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Effect of Sprouty2 Downregulation on MicroRNA Expression Profile in HCT116 Colon Cancer Cells

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Effect of Sprouty2 Downregulation on MicroRNA Expression Profile in HCT116 Colon Cancer Cells

Project description:Sprouty proteins are evolutionarily conserved modulators of mitogen-activated protein kinase pathway. Sprouty2 appears to function as a tumor suppressor in cancers, whereas we reported earlier that Sprouty2 functions as an oncogene in colorectal cancer. To further understand the oncogenic potential of Sprouty2 in the colon, microRNA expression profile of colon cancer cells was investigated. Sprouty2 suppression in HCT116 colon cancer cells significantly increased MicroRNA 194-5p. Sprouty2 dependent regulation of microRNA194-5p and its biological targets were studied further for their tumor suppressive actions in reducing epithelial-mesenchymal transition in colorectal cancer. Sprouty2 knockdown was performed by infecting HCT116 cells with three different lentivirus expressing shRNAs against human Sprouty2 mRNA and a control non targeted non-silencing shRNA (Sprouty2 MISSION shRNA Lentiviral Transduction Particles; TRCN 0000007522, TRCN 0000231589, TRCN 0000231588 and a non-targeted shRNA control from Sigma) following lentiviral transduction protocols provided by Sigma. Due to the random integration of the lentivirus into the host genome, varying levels of Sprouty2 gene knockdown was expected in puromycin resistant colonies. Three colonies in triplicate that demonstrated highest to lowest level of Sprouty2 suppression, as assessed by western blotting, were selected. RNA samples from these colonies and one from non-targeted shRNA expressing colony were prepared for microRNA expression profile analysis. Pooled RNA samples from each group were shipped to Exiqon for microRNA profiling based on miRCURY LNATM array technology.

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Project description:The role of SPROUTY2 (SPRY2) in human colon cancer is controversial. Our data support a tumorigenic action of SPRY2. We use microarrays to identify SPRY2 target genes in human SW480 ADH colon carcinoma cell line. RNA was obtained from SW480 ADH cells, Mock transfected or transfected with WT or two differents SPRY2 genes mutants. Hybridization was performed on Affymetrix microarrays. We performed three independent experiments. Each experiment was conducted in triplicate.

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Loss of Elp3 impairs the immune response to helminths by blocking intestinal tuft cell differentiation

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Project description:While the lung bears significant regenerative capacity, severe viral pneumonia can chronically impair lung function by triggering dysplastic remodeling. The connection between these enduring changes and chronic disease remains poorly understood. We recently described the emergence of tuft cells within Krt5+ dysplastic regions after influenza injury. Using bulk and single cell transcriptomics, we characterized and delineated multiple distinct tuft cell populations that arise following influenza clearance. Distinct from intestinal tuft cells which rely on Type 2 immune signals for their expansion, neither IL-25 nor IL-4Ra signaling are required to drive tuft cell development in dysplastic/injured lungs. Furthermore, tuft cells were also observed upon bleomycin injury, suggesting that their development may be a general response to severe lung injury. While intestinal tuft cells promote growth and differentiation of surrounding epithelial cells, in the lungs of tuft cell deficient mice, Krt5+ dysplasia still occurs, goblet cell production is unchanged, and there remains no appreciable contribution of Krt5+ cells into more regionally appropriate alveolar Type 2 cells. Together, these findings highlight unexpected differences in signals necessary for lung tuft cell amplification and establish a framework for future elucidation of tuft cell functions in pulmonary health and disease.

2022-09-14 | GSE197162 | GEO

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