MUC2 is the prominent colonic mucin expressed in ulcerative colitis.

Tytgat, Kristien M. A. J.; Opdam, Frank J.M.; Einerhand, Alexandra W. C.; Büller, Hans A.; Dekker, Jan

doi:10.1136/gut.38.4.554

Cited by 70 publications

(68 citation statements)

References 46 publications

(16 reference statements)

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“…36 MUC2 protein synthesis, secretion, and sulfation are decreased in active UC, although Myerscough et al found MUC2 and MUC4 mRNA to be similar to controls. 18,[37][38][39][40] MUC1 and MUC3 mRNA were reduced in UC in this study. 40 In CD, decreased mRNA levels of MUC3, MUC4, and MUC5B were found in healthy and inflamed ileal mucosa compared with controls, whereas MUC1 mRNA was reduced in inflamed mucosa only.…”

Section: Intestinal Mucinsmentioning

confidence: 44%

Genetics of the innate immune response in inflammatory bowel disease

Limbergen

Russell

Nimmo

et al. 2007

Inflammatory Bowel Diseases

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The discovery of nucleotide-binding oligomerization domain 2/caspase recruitment domain-containing protein 15 (NOD2/CARD15) as the first susceptibility gene in Crohn's disease (CD) has shifted the focus of research into the pathogenesis of inflammatory bowel disease (IBD) firmly to the innate immune response and the integrity of the epithelial barrier. The subsequent implication in IBD of variant alleles of OCTN, DLG5, MDR1, and TLRs has provided further support for a new, more complex model of innate immunity function in the gastrointestinal tract. In this review, we examine the recent advances in our understanding of the influence of genetics of the innate immune response on IBD. We will focus on germline variation of genes encoding pathogen-recognition receptors, proteins involved in epithelial homeostasis and secreted antimicrobial proteins.

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Section: Intestinal Mucinsmentioning

confidence: 44%

Genetics of the innate immune response in inflammatory bowel disease

Limbergen

Russell

Nimmo

et al. 2007

Inflammatory Bowel Diseases

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“…26 However, Tytgat et al did not find any alterations in the MUC2 mRNA levels. [27][28][29] The amounts of MUC2 could potentially be of importance in UC pathogenesis since it might be related to our observation of an inner mucus layer built around the MUC2 network, acting as a barrier to keep the colon bacteria at a distance from the epithelia. 4 Lack of Muc2, as in Muc2 null mice, 4,30 or mutations in Muc2 31 cause spontaneous colitis and later on colon cancer.…”

Section: Discussionmentioning

confidence: 93%

Altered O-glycosylation profile of MUC2 mucin occurs in active ulcerative colitis and is associated with increased inflammation

Larsson

Karlsson

Crespo

et al. 2011

Inflammatory Bowel Diseases

270

218

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“…Similarly, the MUC2 and MUC3 genes are expressed in ulcerative colitis and Crohn's disease at levels similar to those in normal mucosa, despite goblet cell depletion (32)(33)(34). Of note, in these settings, MUC genes are expressed in the goblet cells and the columnar cells of the surface epithelium (34), and trefoil peptides, including ITF, are expressed ectopically in a so-called ulcer-associated cell lineage (35,36).…”

Section: Discussionmentioning

confidence: 99%

A paradoxical reduction in susceptibility to colonic injury upon targeted transgenic ablation of goblet cells

Itoh¹,

Beck²,

Inoue³

et al. 1999

J. Clin. Invest.

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MethodsPreparation of mITF promoter. To obtain a sufficiently large segment of 5′ flanking promoter region to confer goblet cell-specific expression of the transgene, a Hiroshi Itoh and Paul L. Beck contributed equally to this work.Received for publication January 5, 1999, and accepted in revised form October 21, 1999.Goblet cells are the major mucus-producing cells of the intestine and are presumed to play an important role in mucosal protection. However, their functional role has not been directly assessed in vivo.In initial studies, a 5′ flanking sequence of the murine intestinal trefoil factor (ITF) gene was found to confer goblet cell-specific expression of a transgene. To assess the role of goblet cells in the intestine, we generated transgenic mice in which ∼60% of goblet cells were ablated by the expression of an attenuated diphtheria toxin (DT) gene driven by the ITF promoter; other cell lineages were unaffected. We administered 2 exogenous agents, dextran sodium sulfate (DSS) and acetic acid, to assess the susceptibility of mITF/DT-A transgenic mice to colonic injury. After oral administration of DSS, 55% of control mice died, whereas DT transgenic mice retained their body weight and less than 5% died. Similarly, 30% of the wild-type mice died after mucosal administration of acetic acid, compared with 3.2% of the transgenic mice. Despite the reduction in goblet-cell number, the total amount of ITF was increased in the mITF/DT-A transgenic mice, indicating inducible compensatory mechanisms. These results suggest that goblet cells contribute to mucosal protection and repair predominantly through production of trefoil peptides. Construction of transgene and generation of β-galactosidase ITF transgenic mice. The β-galactosidase gene was obtained from pSV-β-galactosidase vector (Promega Corp., Madison, Wisconsin, USA) by digestion with BamHI and HindIII. The resulting 3.7 kb of β-galactosidase gene was inserted into the BamHI and HindIII sites of pBluescript II KS(+). The 6.3 kb of XhoI-digested 5′ end of the mITF promoter was then inserted into XhoI sites of pBluescript II KS(+) containing the β-galactosidase gene. The resulting plasmid was digested with BamHI, yielding a 10-kb DNA fragment consisting of the 6.35-kb mITF promoter followed by the β-galactosidase gene (3.7 kb). This fragment was gel purified, dialyzed, and injected into the mouse oocytes. The resulting offspring were screened both by Southern blotting (using the above β-galactosidase fragment as a probe) and by PCR using the following primers directed at the inserted β-galactosidase gene: sense: 5′-CCTGAGGCCGATACTGTCGTC-3′; antisense: 5′-CCAGATAACTGCCGTCACTCC-3′. PCR was performed according to the manufacturer's guidelines (Promega Corp.) using 0.5 µL of Taq DNA polymerase (Promega Corp.) in a 50-µL reaction containing 1.5 mM MgCl 2 , 0.2 mM dNTP, 0.8 µM of each primer, and approximately 1 µg of extracted tail DNA. PCR conditions included an initial 10 minutes at 95°C followed by 36 cycles each of 95°C for 1 minute, 58°C for 1 minute, 72°C f...

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MUC2 is the prominent colonic mucin expressed in ulcerative colitis.

Cited by 70 publications

References 46 publications

Genetics of the innate immune response in inflammatory bowel disease

Genetics of the innate immune response in inflammatory bowel disease

Altered O-glycosylation profile of MUC2 mucin occurs in active ulcerative colitis and is associated with increased inflammation

A paradoxical reduction in susceptibility to colonic injury upon targeted transgenic ablation of goblet cells

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