Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection.

Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. Research Abstract Details 

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Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. Abstract Text:

Maria Van der Sluis,Barbara A E De Koning,Adrianus C J M De Bruijn,Anna Velcich,Jules P P Meijerink,Johannes B Van Goudoever,Hans A ,Jan Dekker,Isabelle Van Seuningen,Ingrid B Renes,Alexandra W C Einerhand,

BACKGROUND & AIMS: Expression of mucin MUC2, the structural component of the colonic mucus layer, is lowered in inflammatory bowel disease. Our aim was to obtain insight in the role of Muc2 in epithelial protection. METHODS: Muc2 knockout (Muc2(-/-)) and Muc2 heterozygous (Muc2(+/-)) mice were characterized and challenged by a colitis-inducing agent, dextran sulfate sodium (DSS). We monitored clinical symptoms, intestinal morphology, and differences in intestine-specific protein and messenger RNA levels. RESULTS: The Muc2(-/-) mice showed clinical signs of colitis (as of 5 weeks), aggravating as the mice aged. Microscopic analysis of the colon of Muc2(-/-) mice showed mucosal thickening, increased proliferation, and superficial erosions. Colonic goblet cells in the Muc2(-/-) mice were negative for Muc2, but trefoil factor 3 was still detectable. In Muc2(-/-) mice, transient de novo expression of Muc6 messenger RNA was observed in the distal colon. On day 2 of DSS treatment, the histologic damage was more severe in Muc2(+/-) versus wild-type (Muc2(+/+)) mice, but the disease activity index was not yet different. By day 7, the disease activity index and histologic score were significantly elevated in Muc2(+/-) versus Muc2(+/+) mice. The disease activity index of the Muc2(-/-) mice was higher (versus both Muc2(+/+) and Muc2(+/-) mice) throughout DSS treatment. The histologic damage in the DSS-treated Muc2(-/-) mice was different compared with Muc2(+/+) and Muc2(+/-) mice, with many crypt abscesses instead of mucosal ulcerations. CONCLUSIONS: This study shows that Muc2 deficiency leads to inflammation of the colon and contributes to the onset and perpetuation of experimental colitis.

Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. Publishing Authors By Initials

M Van der Sluis,BA De Koning,AC De Bruijn,A Velcich,JP Meijerink,JB Van Goudoever,HA ,J Dekker,I Van Seuningen,IB Renes,AW Einerhand,

For similar nucleic acids, nucleotides, and nucleosides: nucleic acids: rna: rna, messenger research abstracts see: nucleic acids, nucleotides, and nucleosides: nucleic acids: rna: rna, messenger research

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Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Gastroenterology

VOLUME: 131

Page Numbers: 117-29

Journal Abbreviation: Gastroenterology

ISSN: 0016-5085

DAY: 30

MONTH: Jul

YEAR: 2006

Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. Information

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LANGUAGE: eng

NlmUniqueID: 374630

Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. Keywords Mesh Terms:

KEYWORDS: RNA, Messenger

MESH TERMS: genetics

Chemical & Substance for Abstract: Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. Information

Substance Name: Dextran Sulfate

Registry Number: 9042-14-2

Grant and Affiliation Information for Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection.

AFFILIATION: Division of Neonatology, Department of Pediatrics, Erasmus MC and Sophia Children's Hospital, Rotterdam, The Netherlands.

Country: United States

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MEDLINETA: Gastroenterology

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