Trefoil factors: initiators of mucosal healing

Taupin, Douglas; Podolsky, Daniel K.

doi:10.1038/nrm1203

Cited by 559 publications

(502 citation statements)

References 127 publications

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“…2 Studies are underway to determine whether it is possible to either prevent or lessen the impact of preservation injury to the biliary tract using pretreatment of the donor with either IL-6 or rTFF3. 17 In addition, TFF expression is tightly linked with inflamma-tion and gastric carcinogenesis. Similar associations would be expected for the biliary tree.…”

Section: Discussionmentioning

confidence: 99%

“…1,17 Because it is difficult to directly observe BEC wound healing in the biliary tree under dynamic conditions in vivo, we relied on a wound healing assay in vitro. In vitro IL-6 ϩ/ϩ BECs consistently showed significantly better migration and wound healing than IL-6 Ϫ/Ϫ BECs.…”

Section: Discussionmentioning

confidence: 99%

“…TFF also contributes to restitution of epithelial barriers in the gastrointestinal tract by promoting epithelial cell migration in wound healing assays. 17 Initial analyses were performed in vitro, using complete serum-free medium (C-SFM), a medium that stimulates BEC IL-6 production 13,18 and magnifies the differences between IL-6 ϩ/ϩ and IL-6 Ϫ/Ϫ BECs related primarily to BEC IL-6 production. Isolating the BECs in culture also removes potential confounding paracrine influences of other growth factors and cytokines that are produced by peribiliary stromal and hematopoietic cells after BDL in vivo.…”

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confidence: 99%

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Regulation and Function of Trefoil Factor Family 3 Expression in the Biliary Tree

Nozaki

Lunz

Specht

et al. 2004

The American Journal of Pathology

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Microarray analysis identified trefoil factor family 3 (TFF3) as a gene expressed in biliary epithelial cells (BECs), regulated by interleukin (IL)-6, and potentially involved in biliary pathophysiology. We therefore studied the regulation and function of BEC TFF3, in vitro and in vivo in IL-6 ؉/؉ and IL-6 ؊/؊ mice subjected to chronic bile duct ligation for 12 weeks. In vitro studies showed that IL-6 wild-type (IL-6 ؉/؉ ) BECs expressed higher TFF3 mRNA and protein levels than IL-6-deficient (IL-6 ؊/؊ ) BECs. BEC TFF3 expression is dependent primarily on signal transducer and activator of transcription (STAT3) signaling, but the reciprocal negative regulation known to exist between the intracellular IL-6/gp130 signaling pathways, STAT3 and mitogen-activated protein kinase (MAPK), importantly contributes to BEC TFF3 expression. Specifically blocking STAT3 activity with a dominant-negative molecule or treatment with a growth factor such as hepatocyte growth factor, which increases MAPK signaling, decreases BEC TFF3 expression. In contrast, specifically blocking MAPK activity with PD98059 significantly increased BEC TFF3 expression. Higher BEC TFF3 levels in IL-6 ؉/؉ BECs were associated with significantly better migration than IL-6 ؊/؊ BECs in a wound-healing assay and defective IL-6 ؊/؊ BEC migration was reversed with exogenous TFF3. In vivo, hepatic TFF3 mRNA and protein expression was limited to BECs and dependent significantly on STAT3 signaling, but was influenced by other factors present after bile duct ligation. Com-

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Regulation and Function of Trefoil Factor Family 3 Expression in the Biliary Tree

Nozaki

Lunz

Specht

et al. 2004

The American Journal of Pathology

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“…TFFs are efficient motogenic agents with beneficial effects on the gastrointestinal epithelia, promoting wound healing and mucosal restitution after local injury. Although some studies argue for a therapeutic potential of TFFs in mucosal injury and wound healing (Babyatsky et al, 1996;Taupin and Podolsky, 2003), recent advances in the field support their adverse effects during chronic inflammation and cancer progression. We have recently proposed that TFF1 exerts dual roles in the digestive mucosa.…”

Section: Introductionmentioning

confidence: 99%

Induction of the adenoma-carcinoma progression and Cdc25A-B phosphatases by the trefoil factor TFF1 in human colon epithelial cells

et al. 2006

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“…Trefoil factors (TFFs) are a family of 3 cysteine‐rich proteins, TFF1, TFF2 and TFF3, having roles in mucosal repair and protection against GI insult 96. Studies have demonstrated that TFFs interact with mucins to aid mucus gel integrity 92.…”

Section: Gi Nematode Infection and Mucus‐associated Proteinsmentioning

confidence: 99%

A sticky end for gastrointestinal helminths; the role of the mucus barrier

Sharpe

Thornton

Grencis

2018

Parasite Immunology

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SummaryGastrointestinal (GI) nematodes are a group of successful multicellular parasites that have evolved to coexist within the intestinal niche of multiple species. It is estimated that over 10% of the world's population are chronically infected by GI nematodes, making this group of parasitic nematodes a major burden to global health. Despite the large number of affected individuals, there are few effective treatments to eradicate these infections. Research into GI nematode infections has primarily focused on defining the immunological and pathological consequences on host protection. One important but neglected aspect of host protection is mucus, and the concept that mucus is just a simple barrier is no longer tenable. In fact, mucus is a highly regulated and dynamic‐secreted matrix, underpinned by a physical hydrated network of highly glycosylated mucins, which is increasingly recognized to have a key protective role against GI nematode infections. Unravelling the complex interplay between mucins, the underlying epithelium and immune cells during infection are a major challenge and are required to fully define the protective role of the mucus barrier. This review summarizes the current state of knowledge on mucins and the mucus barrier during GI nematode infections, with particular focus on murine models of infection.

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Trefoil factors: initiators of mucosal healing

Cited by 559 publications

References 127 publications

Regulation and Function of Trefoil Factor Family 3 Expression in the Biliary Tree

Regulation and Function of Trefoil Factor Family 3 Expression in the Biliary Tree

Induction of the adenoma-carcinoma progression and Cdc25A-B phosphatases by the trefoil factor TFF1 in human colon epithelial cells

A sticky end for gastrointestinal helminths; the role of the mucus barrier

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