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IRF6 — MUC20

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Choi et al., Hepatology 1999 : The aim of the present study was to determine whether lipopolysaccharides (LPS) from different bacteria are capable of stimulating mucin secretion by cultured dog gallbladder epithelial ( DGBE ) cells, and to investigate the mechanism by which LPS stimulate mucin secretion ... LPS , derived from Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa ( 200 microg/mL ), all caused an increase in mucin secretion by the DGBE cells, without causing concomitant cell lysis ... Addition of the nitric oxide ( NO ) -releasing compound, NOR-4 ( 0.125-1 mmol/L ), to the cells did not result in increased mucin secretion, and the NO synthase inhibitor, Nomega-nitro-L-arginine methyl ester ( L-NAME ) ( 4 or 10 mmol/L ), did not inhibit the LPS stimulated mucin secretion ... Exogenous tumor necrosis factor alpha (TNF-alpha) ( 1-10 ng/mL ) did cause a minor increase in mucin secretion by the DGBE cells, but the effect of LPS from E. coli on mucin secretion could not be inhibited by preincubation with a TNF-alpha antibody ( 10 microg/mL ) ... We conclude that LPS stimulates mucin secretion by the gallbladder epithelium
Slomiany et al., Biochem Biophys Res Commun 2002 : Inhibition of ERK with PD98059 accelerated ( up to 36.1 % ) the LPS induced decrease in mucin synthesis, and caused further enhancement in caspase-3 activity and apoptosis ... Blockade of p38 kinase with SB203580 produced reversal in the LPS induced reduction in mucin synthesis, and substantially countered the LPS induced increases in caspas-3 activity and apoptosis
Slomiany et al., J Physiol Pharmacol 2003 : The impedance by ciglitazone of the LPS induced changes in mucin synthesis was blocked by PD98059, an inhibitor of extracellular signal regulated kinase ( ERK ), as well as wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K)
Slomiany et al., IUBMB Life 2003 (Helicobacter Infections) : Using gastric mucosal cells in culture, we show that activation of PPARgamma with a specific synthetic agonist, ciglitazone, prevents in a dose dependent fashion ( up to 90.2 % ) the LPS induced reduction in mucin synthesis, and the effect is reflected in a marked decrease in the LPS induced apoptosis ( 72.4 % ), NO generation ( 80.1 % ), and the expression of NOS-2 activity ( 90 % ) ... The impedance by ciglitazone of the LPS induced reduction in mucin synthesis was blocked by wortmannin, a specific inhibitor of P13K and PD98059, an inhibitor of ERK
Shao et al., Proc Natl Acad Sci U S A 2003 : PMA, PA sup, and LPS increased MUC5AC gene expression and mucin protein production, effects that were prevented by pretreatment with AG1478, a selective inhibitor of EGFR phosphorylation and by preincubation with an EGFR neutralizing Ab or with a TGF-alpha neutralizing Ab, implicating ligand ( TGF-alpha ) -dependent EGFR phosphorylation in mucin production ... Knockdown of TACE inhibited PMA-, PA sup-, and LPS induced TGF-alpha shedding, EGFR phosphorylation, and mucin production
Slomiany et al., Biochem Biophys Res Commun 2003 (Bacteroidaceae Infections) : The impedance by leptin of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of PI3K, which also obviated the inhibitory effect of leptin on the LPS induced upregulation in apoptosis, caspase-3 activity, and NO generation ... A potentiation in the impedance by leptin of the LPS induced apoptosis, caspase-3 activity, and NO generation was, however, attained with NOS-2 inhibitor, 1400W, that also caused further enhancement in the impedance by leptin of the LPS detrimental effect on mucin synthesis
Slomiany et al., IUBMB Life 2004 (Gastritis...) : The impedance by BN52020 of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of phosphatidylinositol 3-kinase ( P13K ), which also obviated the inhibitory effect of BN52020 on the LPS induced upregulation in apoptosis, TNF-alpha, and NO generation ... A reduction in the impedance by BN52020 of the LPS detrimental effect on mucin synthesis was also attained with cNOS inhibitor, L-NNA, whereas NOS-2 inhibitor, 1400W caused a potentiation in the impedance effect of BN52020 ... However, while 1400W and BN52020 countered the potentiating effect of wortmannin on the LPS induced decrease in mucin synthesis, a further exacerbation of the potentiating effect of wortmannin was attained in the presence of cNOS inhibitor, L-NNA
Kim et al., Ann N Y Acad Sci 2003 (Adenocarcinoma...) : Blockade of p38 mitogen activated kinase ( MAPK ) produced reversal in the LPS induced reduction in mucin synthesis and apoptosis in gastric epithelial cells
Slomiany et al., Inflammopharmacology 2003 : A pronounced prevention ( 88.2 % ) in the LPS induced PGE ( 2 ) release and the diminished COX-2 protein expression was also attained with the COX-2-selective inhibitor NS-398, but the effect was not associated with the impedance of the LPS inhibitory effect on mucin synthesis ... Activation of PPARgamma with a specific synthetic agonist, ciglitazone, countered ( up to 90.2 % ) the LPS induced reduction in mucin synthesis in a concentration dependent manner, and this effect of the agent was reflected in a marked decrease in COX-2 and NOS-2 protein expression, reduction ( up to 72.4 % ) in apoptosis and a decline ( up to 84.1 % ) in PGE ( 2 ) generation and NOS-2 activity ( up to 90 % )
Slomiany et al., J Physiol Pharmacol 2004 (Disease Models, Animal) : Using primary culture of mucous acinar cells of sublingual salivary gland, we show that a specific PAF antagonist, BN52020, prevents in a dose dependent fashion ( up to 83.7 % ) the LPS induced reduction in mucin synthesis, and the effect is reflected in a marked decrease in the LPS induced apoptosis ( 74.8 % ), NO generation ( 82.6 % ), and the expression of TNF-alpha ( 76.1 % ) ... The impedance by BN52020 of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K), which also obviated the inhibitory effect of BN52020 on the LPS induced upregulation in apoptosis, TNF-alpha, and NO. A potentiation in the impedance by BN52020 of the LPS detrimental effect on mucin synthesis was however attained with NOS-2 inhibitor, 1400W, while cNOS inhibitor, L-NNA caused a reduction in the impedance effect of BN52020 ... However, while 1400W and BN52020 countered the potentiating effect of wortmannin on the LPS induced decrease in mucin synthesis, a further exacerbation of the effect of wortmannin occurred in the presence of L-NNA
Slomiany et al., IUBMB Life 2004 : In this study, we report that PPARgamma activation leading to the impedance of P. gingivalis lipopolysaccharide (LPS) inhibitory effect on salivary mucin synthesis requires epidermal growth factor receptor (EGFR) participation ... We show that activation of PPARgamma with a specific agonist, ciglitazone, prevents the LPS induced reduction in mucin synthesis, and the effect is reflected in a marked decrease in apoptosis, caspase-3 activity and NO generation ... The impedance by ciglitazone of the LPS induced reduction in mucin synthesis was countered ( up to 68.9 % ) in a dose dependent fashion by a specific inhibitor of EGFR kinase, PD153035, as well as wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K) ... Moreover, the inhibitory effect of ciglitazone on the LPS induced reduction in mucin synthesis and upregulation in apoptosis, caspase-3 activity, and NO generation was blunted by a selective inhibitor of tyrosine kinase Src, PP2, responsible for ligand independent EGFR transactivation ... These findings indicate that PPARgamma activation leading to the suppression of P. gingivalis LPS inhibition of salivary mucin synthesis involves Src kinase dependent EGFR transactivation
Slomiany et al., Inflammopharmacology 2004 : In this study, we report that PPARgamma activation leading to the impedance of Helicobacter pylori lipopolysaccharide (LPS) inhibitory effect on salivary mucin synthesis requires epidermal growth factor receptor (EGFR) participation ... Using gastric mucosal cells in culture, we show that activation of PPARgamma with a specific agonist, ciglitazone, prevents the LPS induced reduction in mucin synthesis, and the effect is reflected in a marked decrease in apoptosis, caspase-3 activity and NO generation ... The impedance by ciglitazone of the LPS induced reduction in mucin synthesis was blunted ( up to 65.8 % ) in a concentration dependent fashion by a specific inhibitor of EGFR kinase, PD153035, as well as the PPARgamma antagonist BADGE, and wortmannin, an inhibitor of PI3K ... Moreover, the inhibitory effect of ciglitazone on the LPS induced reduction in mucin synthesis and upregulation in apoptosis, caspase-3 activity and NO generation was countered by PP2, a selective inhibitor of tyrosine kinase Src responsible for ligand independent EGFR transactivation
He et al., Acta Pharmacol Sin 2004 : To examine the effects of rhinovirus and lipopolysaccharide (LPS) on mucin secretion from bronchial tissue and epithelial cells in vitro ... LPS 100 mg/L was able to provoke up to approximately 19 % and 54 % increase in DBA and MUC5AC mucin release over baseline, respectively from HSBTF, and 3.1 % and 57 % increase from HBEC at 20 h. Soybean trypsin inhibitor ( SBTI ) 30 mg/L was able to inhibit LPS induced mucin release from HSBTF and HBEC ... LPS can induce MUC5AC mucin release from HSBTF and HBEC
Slomiany et al., IUBMB Life 2004 : Using mucous cells of sublingual salivary gland, we show that P. gingivalis lipopolysaccharide (LPS) inhibitory effect on salivary mucin synthesis is accompanied by a marked increase in ET-I generation and the enhancement in ECE-1 activity ... The LPS induced reduction in mucin synthesis, furthermore, was countered by PD153035 ( 76.8 % ), a specific inhibitor of EGFR kinase as well as PP2 ( 54.7 % ), a selective inhibitor of tyrosine kinase Src responsible for ligand independent EGFR transactivation ... Our findings are the first to demonstrate that P. gingivalis LPS detrimental effect on salivary mucin synthesis is intimately linked to the events controlled by EGFR transactivation, triggered by upregulation in ECE-1, enhancement in ET-1 production, and G protein coupled ETA receptor activation
Slomiany et al., IUBMB Life 2005 : The impedance by leptin of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of PI3K, as well as by ERK inhibitor, PD98059
Slomiany et al., Scand J Gastroenterol 2005 : Inhibition of ECE-1 with phosphoramidon not only led to the impedance of LPS induced ET-1 generation, but also countered the detrimental effect of LPS on mucin synthesis ... Moreover, the LPS inhibitory effect on mucin synthesis was blocked by ET ( A ) receptor antagonist BQ610, but not by ET ( B ) receptor antagonist BQ788
Baginski et al., Am J Respir Cell Mol Biol 2006 (Carcinoma, Mucoepidermoid) : We demonstrated that cigarette smoke extract (CSE) synergistically increased gene expression and protein production of MUC5AC mucin induced by LPS or TNF-alpha in human airway epithelial NCI-H292 cells
Slomiany et al., Inflammopharmacology 2006 : Using mucous cells of sublingual gland, we show that P. gingivalis LPS detrimental effect on salivary mucin synthesis, associated with up-regulation in PAF and endothelin-1 (ET-1) generation, was subject to suppression by a specific inhibitor of cPLA2, MAFP ... Moreover, the LPS induced changes in mucin synthesis and ET-1 generation were countered by PAF receptor antagonist, BN52020 ... The inhibition by PAF antagonist of the LPS induced reduction in mucin synthesis was countered by wortmannin, an inhibitor of PI3K, as well as by ERK inhibitor, PD98059 ... The findings are the first to demonstrate that P. gingivalis LPS detrimental effect on salivary mucin synthesis involves ERK dependent cPLA2 activation that leads to up-regulation in PAF production and ET-1 generation
Slomiany et al., J Physiol Pharmacol 2007 : On the other hand, the prevention by leptin of the LPS detrimental effect on mucin synthesis was subject to suppression by wortmannin, an inhibitor of PI3K as well as the inhibitor of ERK, PD98059 ... Moreover, potentiation in the effect of leptin on the LPS induced decrease in mucin synthesis was attained with cPLA(2) inhibitor, MAFP as well as PAF receptor antagonist, BN52020
Hauber et al., J Endotoxin Res 2007 (Inflammation) : LPS induced mucin expression in human sinus mucosa can be attenuated by hCLCA inhibitors ... We also investigated the effect of NFA and MSI-2216 on LPS induced mucin up-regulation ... These data suggest that hCLCA1 may play a role in LPS induced mucin expression in human airway mucosa
Rhee et al., Eur Respir J 2008 : MUC5AC mucin synthesis and the expression of the MUC5AC gene were increased by LPS in rats or TNF-alpha in NCI-H292 cells ; these effects were inhibited by fudosteine treatment
Antonela Antoniu et al., Expert Opin Investig Drugs 2009 : Both LPS and TNF-alpha increased MUC5AC mucin production in vivo and in vitro, respectively, and fudosteine was found to reduce it by partially interfering with the kinase mediated inflammation pathway that activates the MUC5AC gene
Slomiany et al., International journal of inflammation 2011 : In this study, using rat sublingual gland acinar cells, we report that P. gingivalis LPS induced impairment in mucin synthesis and associated suppression in Akt kinase activity were accompanied by a decrease in constitutive nitric oxide synthase ( cNOS ) activity and an induction in inducible nitric oxide synthase (iNOS) expression
Moran et al., Aliment Pharmacol Ther 1996 (Helicobacter Infections) : In vitro observations of inhibition of sulphated mucin synthesis and stimulation of pepsinogen secretion by LPS suggest new mechanisms for H. pylori induced mucosal damage