Increased susceptibility to colitis and colorectal tumors in mice lacking core 3–derived O-glycans (original) (raw)

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Article| May 21 2007

Guangyu An,

1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation

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Bo Wei,

4Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095

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Baoyun Xia,

5Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322

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J. Michael McDaniel,

1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation

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Tongzhong Ju,

5Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322

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Richard D. Cummings,

5Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322

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Jonathan Braun,

4Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095

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Lijun Xia

1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation

2Department of Biochemistry and Molecular Biology,

3Oklahoma Center for Medical Glycobiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104

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Guangyu An

1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation

Bo Wei

4Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095

Baoyun Xia

5Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322

J. Michael McDaniel

1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation

Tongzhong Ju

5Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322

Richard D. Cummings

5Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322

Jonathan Braun

4Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095

Lijun Xia

1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation

2Department of Biochemistry and Molecular Biology,

3Oklahoma Center for Medical Glycobiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104

Abbreviations used: AOM, azoxymethane; C3GnT, core 3 β1,3-N-acetylglucosaminyltransferase; DSS, dextran sodium sulfate; HRP, horseradish peroxidase; IBD, inflammatory bowel disease; IEL, intraepithelial lymphocyte; ITF, intestinal trefoil factor; LPL, lamina propria lymphocyte; O-glycans, O-linked oligosaccharides; PAS, periodic acid-Schiff's reagent.

Received: September 07 2006

Accepted: April 26 2007

Online ISSN: 1540-9538

Print ISSN: 0022-1007

The Rockefeller University Press

2007

J Exp Med (2007) 204 (6): 1417–1429.

Altered intestinal O-glycan expression has been observed in patients with ulcerative colitis and colorectal cancer, but the role of this alteration in the etiology of these diseases is unknown. O-glycans in mucin core proteins are the predominant components of the intestinal mucus, which comprises part of the intestinal mucosal barrier. Core 3–derived O-glycans, which are one of the major types of O-glycans, are primarily expressed in the colon. To investigate the biological function of core 3–derived O-glycans, we engineered mice lacking core 3 β1,3-N-acetylglucosaminyltransferase (C3GnT), an enzyme predicted to be important in the synthesis of core 3–derived O-glycans. Disruption of the C3GnT gene eliminated core 3–derived O-glycans. C3GnT-deficient mice displayed a discrete, colon-specific reduction in Muc2 protein and increased permeability of the intestinal barrier. Moreover, these mice were highly susceptible to experimental triggers of colitis and colorectal adenocarcinoma. These data reveal a requirement for core 3–derived O-glycans in resistance to colonic disease.

The Rockefeller University Press

2007

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