Disease relevance of Tff3

• CONCLUSION: Intrauterine ischemia can result in an early decrease of ITF mRNA expression [1].
• CONCLUSIONS: This study has shown that hTFF2 enhances the rate of colonic epithelial repair, and reduces local inflammation in a rat model of colitis, and suggests that luminal application of trefoil peptides may have therapeutic potential in the treatment of inflammatory bowel disease [2].
• In the present study, we expressed mature rat ITF (rITF) with pXa (a prokaryotic expression vector) in Escherichia coli to generate a biotinylated rITF fusion protein (bTag-ITF) [3].
• Trefoil factor family-3 is associated with aggressive behavior of colon cancer cells [4].
• Effect of omeprazole-induced achlorhydria on trefoil peptide expression in the rat stomach [5].

Psychiatry related information on Tff3

• When compared with the T group, the OS group showed decreased anorexia and body weight loss; reduced bowel wall thickening and longitudinal extension of necrotic lesions; downregulated colonic expression of interleukin 1beta, inducible nitric oxide synthase, cyclooxygenase 2, and mucin 3; and increased trefoil factor 3 [6].

High impact information on Tff3

• CONCLUSIONS: Topical trefoil peptides protect the gastric mucosa against ethanol- and indomethacin-induced gastric injuries [7].
• Oral trefoil peptides protect against ethanol- and indomethacin-induced gastric injury in rats [7].
• BACKGROUND & AIMS: The trefoil factors, a family of proteins abundantly expressed in gastrointestinal mucous cells, protect the epithelium in vitro [7].
• RESULTS: Oral rHSP and ITF markedly protected against both ethanol- and indomethacin-induced gastric injury (P < 0.005 at doses of 1-15 mg/rat) when given up to 2 hours before injury; no protection was noted by intraperitoneal rHSP against ethanol injury [7].
• Spasmolytic polypeptide: a trefoil peptide secreted by rat gastric mucous cells [8].

Chemical compound and disease context of Tff3

• In the first experiment, gastric gavage of troglitazone (PPARgamma ligand, 10 or 100 mg/kg body weight) or bezafibrate (PPARalpha ligand, 10 or 100 mg/kg body weight) inhibited colitis induced by dextran sodium sulfate (DSS) and lowered trefoil factor-2 content in colonic mucosa [9].
• cDNA cloning of rat pS2 peptide and expression of trefoil peptides in acetic acid-induced colitis [10].
• Protection by ITF 1300, a heparin ion-pair complex, against arrhythmias induced by regional ischemia and reperfusion in the isolated rat heart: possible mechanism of action [11].
• Epithelial proliferation, cell death, and gene expression in experimental colitis: alterations in carbonic anhydrase I, mucin MUC2, and trefoil factor 3 expression [12].
• Effects of topical treatment of sodium butyrate and 5-aminosalicylic acid on expression of trefoil factor 3, interleukin 1beta, and nuclear factor kappaB in trinitrobenzene sulphonic acid induced colitis in rats [13].

Biological context of Tff3

• Previous work had localized expression of ITF primarily within goblet cells in the small and large bowel, making it a candidate gene for the study of the molecular basis of intestinal and goblet cell-specific gene expression [14].
• The pattern of goblet cell-associated selective transcription required only 153 base pairs of the rat ITF 5'-flanking sequence [14].
• Intestinal trefoil factor (TFF3) is essential in regulating cell migration and maintaining mucosal integrity in gastrointestinal tract [15].
• Reduction of PSP by GSH is not necessary for this response, suggesting that the trefoil receptor or its signal transduction is GSH sensitive [16].
• Intestinal trefoil factor (ITF), a small peptide secreted by intestinal goblet cells, maintains mucosal integrity and promotes epithelial wound healing [3].

Anatomical context of Tff3

• Both peptides are distributed in the apical secretory compartment of antral mucus cells (SP) and goblet cells (ITF), and on the lumenal surface [17].
• ITF (7 kDa) is highly expressed throughout the small intestine [17].
• ITF and PCNA may play an important role in the damage and repair of intestinal mucosa [1].
• BACKGROUND: The trefoil peptides are major secretory products of mucus cells of the gastrointestinal tract and show increased expression after inflammatory or ulcerative damage [2].
• Using an oligonucleotide derived from N-terminal amino acid sequencing of a transformed growth-inhibiting protein, a cDNA was cloned from rat intestinal villus epithelial cells that encodes a protein 81 amino acids in length with the characteristic trefoil peptide cysteine residue motif [18].

Associations of Tff3 with chemical compounds

• Our data suggest that this 50 kDa membrane glycoprotein is a putative receptor for ITF in the gastrointestinal tract [3].
• In contrast to trefoil secretory rates, the steady-state synthesis of both TFF1/pS2 and TFF2/SP was unchanged after omeprazole treatment, implying both a large cellular pool of processed peptide and rapid secretion [5].
• The C3 deposition induced by complement activation was significantly blocked by the treatment with ITF [19].
• We showed that trefoil factor 3 significantly induces the production of prostaglandin E(2) and prostaglandin I(2) in IEC-18 cells (an intestinal epithelial cell line) in a dose dependent manner [20].
• By binding to their specific receptors angiotensin peptides, namely angiotensin (Ang) II, have also been reported to induce the expression of a variety of inducible transcription factors (ITF) of the AP-1 and other families in peripheral organs such as kidney and blood vessels and in specific brain regions [21].

Regulatory relationships of Tff3

• In summary, our results indicate that trefoil factor 3 activates cyclooxygenase-2 in intestinal epithelium to produce prostaglandin I(2) and prostaglandin E(2), which function as survival factors and mediate the cytoprotective action of trefoil factor 3 against oxidant injury [20].

Other interactions of Tff3

• Correlation analyses showed that IMDI had a negative correlation with ITF mRNA and PCNA (r = -0.543, P<0.05; r = -0.794, P<0.01, respectively) [1].
• BACKGROUND: Trefoil peptides are secreted by mucus producing cells in the gastrointestinal tract and are supposed to be involved in oligomerisation processes of the mucin glycoproteins in the lumen [22].
• Prostanoids mediate the protective effect of trefoil factor 3 in oxidant-induced intestinal epithelial cell injury: role of cyclooxygenase-2 [20].
• In the present study, we examined whether the cyclooxygenase pathway is involved in trefoil factor 3 action [20].
• In contrast, expression of the goblet cell markers, Muc2 and trefoil factor 3, and the Paneth cell marker, lysozyme, was maintained after MTX in both PP and NP epithelium [23].

Analytical, diagnostic and therapeutic context of Tff3

• ITF mRNA was detected by RT-PCR [1].
• After ischemia, ITF mRNA was decreased to the minimum (0.59+/-0.032) 24 h after birth, then began to increase higher after 72 h than it was in the control group (P<0.01) [1].
• Molecular cloning of the rat intestinal trefoil factor gene. Characterization of an intestinal goblet cell-associated promoter [14].
• Localization of intestinal trefoil-factor mRNA in rat stomach and intestine by hybridization in situ [24].
• The trefoil pancreatic spasmolytic polypeptide (PSP) was tested for growth activity in vitro on epithelial cells and in vivo following intragastric or intravenous infusion in parenterally fed intact rats [16].

References