Dataset Information

Proteomics of Muc17-deficient mice small intestine epithelial cells

ABSTRACT: To evaluate the impact of Muc17 deletion on other major intestinal mucins, we employed proteomic analysis of isolated Si5 epithelial cells fromMuc17fl/fl and Muc17∆IEC cohoused littermates. Deletion of Muc17 did not result in a compensatory change in the abundance of the gel-forming mucin Muc2 and membrane mucin Muc13.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Epithelial Cell, Small Intestine Epithelium

SUBMITTER: Liisa Arike

LAB HEAD: Liisa Arike

PROVIDER: PXD048896 | Pride | 2025-05-06

REPOSITORIES: Pride

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			Action	DRS
	230130_QExHFx_LA_MS762_01_230min_1.raw	Raw
	230130_QExHFx_LA_MS762_02_230min.raw	Raw
	230130_QExHFx_LA_MS762_03_230min.raw	Raw
	230130_QExHFx_LA_MS762_04_230min.raw	Raw
	230130_QExHFx_LA_MS762_05_230min.raw	Raw

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Publications

MUC17 is an essential small intestinal glycocalyx component that is disrupted in Crohn's disease.

Layunta Elena E Jäverfelt Sofia S van de Koolwijk Fleur C FC Sivertsson Molly M Dolan Brendan B Arike Liisa L Thulin Sara Im SI Vallance Bruce A BA Pelaseyed Thaher T

JCI insight 20241219 3

Crohn's disease (CD) is the chronic inflammation of the terminal ileum and colon triggered by a dysregulated immune response to bacteria, but insights into specific molecular perturbations at the critical bacteria-epithelium interface are limited. Here, we report that the membrane mucin MUC17 protected small intestinal enterocytes against commensal and pathogenic bacteria. In noninflamed CD ileum, reduced MUC17 levels and a compromised glycocalyx barrier allowed recurrent bacterial contact with ...[more]

PMID: 39699961

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Project description:In this study we compared the intestinal mucus phenotype of Clca1-deficient (Clca1-/-) mice and wild-type (WT) controls. The human CLCA1 (chloride channel regulator, calcium-activated) and its murine ortholog mouse CLCA1 (formerly known as CLCA3) are secreted proteins which have been linked to human respiratory diseases such as asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) as well as to the corresponding murine models of these diseases. Common, disease severity-related features are goblet cell hyperplasia, mucus overproduction and disturbed clearance. Neutralization of mouse CLCA1 ameliorates the symptoms in the asthmatic mouse model and restoration of the decreased mouse CLCA1 protein level in a CF mouse model ameliorates the intestinal CF lesions, pointing toward these proteins being potential therapeutic targets. The expression CLCA1 can be induced in airways but this protein is normally expressed and secreted by goblet cells of the intestinal tract in both human and mouse together with the intestinal MUC2 mucin. This makes CLCA1 a major constituent of the extracellular intestinal mucus in which the MUC2 mucin is the main structural component. To study the possible further effects of murine CLCA1 deficiency on Muc2 and on other important components of the mucus, such as Agr2, Fcgbp, Klk and Zg16, a shotgun label-free proteomics study was performed which compared their relative abundance in the mucus layer, showing a tight and significant correlation between WT and Clca1-/- mucus proteins (Pearson r = 0.931, r2 = 0.868, p < 0.0001, based on 809 valid pairs). No significant differences in known mucus protein expression were observed. However, the abundance of CLCA1 in the mucus together with the domain structure suggests a structural role and other methods to reveal the function of these domains might shed light on the overall function in mucus. Because of its abundance in the mucus and the well preserved structure thought a long evolution together with mucus we still speculate that CLCA1 was developed to protect the expressing organism, although the threat is elusive.