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Robust colonic epithelial regeneration and amelioration of colitis via FZD-specific activation of Wnt signaling

ABSTRACT: Robust colonic epithelial regeneration and amelioration of colitis via FZD-specific activation of Wnt signaling

PROVIDER: PRJNA832756 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18942612_1.fastq.gz	Fastqsanger.gz
	SRR18942612_2.fastq.gz	Fastqsanger.gz
	SRR18942613_1.fastq.gz	Fastqsanger.gz
	SRR18942613_2.fastq.gz	Fastqsanger.gz
	SRR18942614_1.fastq.gz	Fastqsanger.gz

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Robust colonic epithelial regeneration and amelioration of colitis via FZD-specific activation of Wnt signaling

Project description:Background and aims: Current management of inflammatory bowel disease (IBD) leaves a clear unmet need to treat the severe epithelial damage. Modulation of Wnt signaling might present an opportunity to achieve histological remission and mucosal healing when treating IBD. Exogenous R-spondin (RSPO), which amplifies Wnt signals by maintaining cell surface expression of Frizzled (FZD) and low-density lipoprotein receptor-related protein (LRP) receptors, helps repair intestine epithelial damage, but it also induces hyperplasia of normal epithelium. Wnt signaling may also be modulated with the recently developed Wnt mimetics, recombinant antibody-based molecules mimicking endogenous Wnts. Methods: We first compared the epithelial healing effects of RSPO2 and a Wnt mimetic with broad Fzd-specificity in an acute Dextran Sodium Sulfate (DSS) mouse colitis model. Guided by Fzd expression patterns in the colon epithelium, we also examined the effects of Wnt mimetics with sub-family Fzd-specificities. Results: In the DSS model, Wnt mimetics repaired damaged colon epithelium and reduced disease activity and inflammation and had no apparent effect on uninjured tissue. We further identified that the FZD5/8 and LRP6 receptor-specific Wnt mimetic, SZN-1326-p, was associated with the robust repair effect. Through a range of approaches including single-cell transcriptome analyses, we demonstrated that SZN-1326-p directly impacted epithelial cells, driving transient expansion of stem and progenitor cells, promoting differentiation of epithelial cells, histologically restoring the damaged epithelium and, secondarily to epithelial repair, reducing inflammation. Conclusion: It is feasible for treating epithelial damage in IBD to design Wnt mimetics such as SZN-1326-p that affect damaged intestine epithelium specifically and restore its physiological functions.

2022-05-19 | GSE201723 | GEO

Robust Colonic Epithelial Regeneration and Amelioration of Colitis via FZD-Specific Activation of Wnt Signaling.

Project description: Not available

| S-EPMC9305022 | biostudies-literature

Transcription profiling of human ulcerative colitis colonic mucosa to define an ulcerative colitis preinflammatory state

Project description:The samples are a part of a study aiming at diagnosing ulcerative colitis from genome-wide gene expression analysis of the colonic mucosa. Colonic mucosal samples were collected as endoscopic pinch biopsies from ulcerative colitis patients and from control subjects. Samples with and without macroscopic signs of inflammation were collected from the patients. Experiment Overall Design: The series contain eight UC samples with macroscopic signs of inflammation, 13 UC smaples without macroscopic signs of inflammation, five control subjects.

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miRNome of colonic crypt stem cells from DSS-induced colitis mice

Project description:To identify potential unique miRs that contribute to shaping the intestinal stemness in colitis, we analyzed the miRNome of colonic crypt stem cells from DSS-induced colitis mice.

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Temporal transcriptional profiles of colonic tissue during DSS-induce colitis

Project description:Inflammation dramatically alters the gut microenvironment. To investigate the transcriptome changes the temporal profile of multiple signaling pathways throughout the progression of colitis, we collected the colonic tissue at a series of time points during DSS colitis for bulk RNA sequencing.

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Effects of deoxycholic acid on gene expression in colonic tissue of colitis mice

Project description:To investigate the roles of deoxycholic acid in the regulation of cell function and gene expression of colonic tissue, we treated colitis mice with deoxycholic acid. Then, we performed gene expression profiling analysis using data obtained from RNA-seq of colonic tissue of colitis mice treated with or without deoxycholic acid.

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TRPM8 inhibits substance P release from primary sensory neurons via PKA/GSK-3beta to protect colonic epithelium in colitis

Project description:Transient receptor potential melastatin 8 (TRPM8) is a cold sensory receptor in primary sensory neurons that regulates various neuronal functions. Substance P (SP) is a pro-inflammatory neuropeptide secreted by the neurons, and it aggravates colitis. However, the regulatory role of TRPM8 in SP release is still unclear. Our study aimed to investigate TRPM8’s role in SP release from primary sensory neurons during colitis and clarify the effect of SP on colonic epithelium. We analyzed inflammatory bowel disease patients’ data from the Gene Expression Omnibus dataset. Dextran sulfate sodium (DSS, 2.5%)-induced colitis in mice, mouse dorsal root ganglion (DRG) neurons, ND7/23 cell line, and mouse or human colonic organoids were used for this experiment. TRPM8, TAC1 and WNT3A expressions were significantly correlated with the severity of ulcerative colitis in patients and DSS-induced colitis in mice. The TRPM8 agonist (menthol) and the SP receptor antagonist (Aprepitant) can attenuate colitis in mice, but the effects were not additive. Menthol promoted calcium ion influx in mouse DRG neurons. TRPM8 inhibited the combination of PKAca from the cAMP signaling pathway and GSK-3β from the Wnt/β-catenin signaling pathway, thereby inhibiting the role of β-catenin in promoting the release of SP from ND7/23 cell line. Long-term stimulation with SP inhibited proliferation and enhanced apoptosis in both mouse and human colonic organoids. Conclusively, TRPM8 inhibits SP release from primary sensory neurons by inhibiting the interaction between PKAca and GSK-3β, thereby inhibiting the role of SP in promoting colonic epithelial apoptosis and relieving colitis.

2023-09-12 | GSE242559 | GEO

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2024-06-01 | GSE249871 | GEO

Chemical-induced colitis lowers mitochondrial bioenergetic function in the colonic epithelium with minimal impacts on the proteome

Project description:Dextran Sulfate Sodium (DSS) is widely used to model colitis due to its ability to disrupt the colonic epithelial barrier and trigger inflammation. While DSS is a valuable tool for studying colitis-related diseases, its impact on mitochondrial bioenergetics and the proteomic landscape of colonic tissue remains poorly understood. To address this gap, we administered 3% DSS in drinking water to C57BL/6J mice and analyzed resected colonic tissue from treated and control mice. Longitudinally opened colon segments were cleaned and subjected to high-resolution respirometry and mass spectrometry-based proteomic profiling. DSS treatment led to a global lowering of mitochondrial respiration, with the most pronounced impairments observed in complex I-supported respiration. Proteomic analysis revealed that these functional deficits occurred largely independently of changes in the mitochondrial proteome, except for an upregulation of NIPSNAP1, a mitophagy-related protein. However, lentiviral knockdown of NIPSNAP1 in HCT116 cells did not rescue the observed bioenergetic defects, suggesting it is not the primary driver. Collectively, our findings show that DSS impairs mitochondrial respiration in the colon—most notably at complex I—without major alterations to the mitochondrial proteome. Given the role of mitochondrial dysfunction in various diseases, these effects should be carefully considered when using DSS-based models to study colitis pathophysiology.

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Gene expression data from colitis-associated colonic tumors of WT vs. MDR1A KO mice

Project description:Human Ulcerative colitis (UC) is characterized by chronic colonic inflammation and has been associated with an increased risk of colorectal carcinoma. Gene and protein expression profiles of ABCB1/MDR1 have been shown to be dysregulated in UC and sporadic colorectal cancer. We demonstrated that in a murine model of colitis-associated tumorigenesis, MDR1A KO mice showed reduced tumor load when compared to wildtype (WT) mice. The aim of this study was to identify gene alterations in colitis-associated tumors in the context of MDR1A deficiency. We used microarrays to assess gene expression profiles of colitis-associated colonic tumors from WT or MDR1A KO mice.

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