Single cell gene expression profile of irradiated small intestinal crypt cells of WT and CREPT KO mice
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PROVIDER: PRJNA951229 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression profiles of irradiated WT and CREPT deleted intestinal epithelium
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Project description:Crypt hyperplasia is a key feature of celiac disease and various other small intestinal inflammatory conditions. By undertaking mass spectrometry-based tissue proteomics of the gut epithelial crypt zone, we found that active celiac disease is characterized by a strong interferon-γ (IFN-γ) signal. This signal, hallmarked by increased expression of MHC molecules, coincides with a markedly reduced expression of proteins associated with fatty acid metabolism. We observed similar crypt hyperplasia and proteomic alterations in wild-type mice treated with IFN-γ, but not in mice that lack the IFN-γ receptor in gut epithelial cells. IFN-γ is thus a driver of crypt hyperplasia in celiac disease by acting directly on crypt epithelial cells. This dataset contains proteomics analysis of crypt compartment samples isolated by laser capture microdissection small intestinal crypt compartment from C57/Bl6 mice injected i.p. with 0-1-2-4-6 or 9 doses interferon gamma every 8 hour.
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Project description:ChIP-seq of CREPT in intestinal crypts
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Project description:Cancer local recurrence increases the mortality of patients, and might be caused by field cancerization, a pre-malignant alteration of normal epithelial cells. It has been suggested that cancer-derived small extracellular vesicles (CDEs) may contribute to field cancerization, but the underlying mechanisms remain poorly understood. In this study, we aim to identify the key regulatory factors within recipient cells under the instigation of CDEs. In vitro experiments were performed to demonstrate that CDEs promote the expression of CREPT in normal epithelial cells. TMT-based quantitative mass spectrometry was employed to investigate the proteomic differences between normal cells and tumor cells. Loss-of-function approaches by CRISPR-Cas9 system were used to assess the role of CREPT in CDEs-induced field cancerization. RNA-seq was performed to explore the genes regulated by CREPT during field cancerization. CDEs promote field cancerization by inducing the expression of CREPT in non-malignant epithelial cells through activating the ERK signaling pathway. Intriguingly, CDEs failed to induce field cancerization when CREPT was deleted, highlighting the importance of CREPT. Transcriptomic analyses revealed that CDEs elicited inflammatory responses, primarily through activation of the TNF signaling pathway. CREPT, in turn, regulates the transduction of downstream signals of TNF by modulating the expression of TNFR2 and PI3K, thereby promoting inflammation-to-cancer transition. CREPT not only serves as a biomarker for field cancerization, but also emerges as a target for preventing the cancer local recurrence.
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Project description:Background & Aims: Liver fibrosis, a serious medical condition with limited therapies, frequently progresses to cirrhosis and other severe complications. Here, we report that cell cycle-related and expression elevated protein in tumor (CREPT) is up-regulated in liver fibrosis. CREPT preferentially enhances transforming growth factor-β (TGF-β)-activated Smad2/3, rather than the canonical Smad2/3-Smad4 complex, thereby facilitating liver fibrosis progression. Methods: We analyzed public transcriptomic and proteomic datasets from patients with liver fibrosis. Human tissue arrays and mouse models of fibrosis were used to investigate CREPT expression patterns. Hepatocyte-specific overexpression (TG-CREPT) and deletion (CREPThep-/-) mice were subjected to acute liver injury (24 h, high-dose CCl4), chronic fibrosis (28 d, low-dose CCl4), and bile duct ligation (BDL) to induce liver fibrosis. Histological, biochemical, and RNA-sequencing (RNA-seq) analyses and CUT&Tag experiments were conducted. Results: CREPT is predominantly enriched in hepatocytes and upregulated in fibrotic liver tissues from patients and mice induced by CCl4 or BDL. Overexpression of CREPT in hepatocytes exacerbates liver injury and fibrosis in mice under acute or chronic CCl4 exposure and BDL challenge. In contrast, hepatocyte-specific deletion of CREPT significantly alleviates liver fibrosis. Mechanistically, CREPT aggravates TGF-β/Smad signaling pathway, preferentially interacting with Smad2/3, but not Smad4, to promote inflammatory responses, and up-regulates fibrogenic genes, including Cebpd, Fosl2 and Fn1. Intriguingly, targeting CREPT with LNP-delivered siRNA (LNP-siCREPT) and GalNAc-delivered siRNA (GalNAc-siCREPT) significantly reduces pre-existing liver fibrosis in mice. Conclusions: Our findings identify a promoting effect of CREPT on liver fibrosis through TGF-β-activated Smad2/3 but not Smad4. Targeting CREPT represents a potential therapeutic strategy for liver fibrosis.
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