• Korean Journal of Microbiology
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• v.28 no.3
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• pp.192-198
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• 1990

To determine whether the muc region of pKM101 and its mutant pSL4 is sufficient for the expression of these phenotypes, muc regions of pKM101 and pSL4 were subcloned onto the highcopy number vector pKB354 and were selected the cloned pJB200 and pJB210. The recombinant plasmids pJB200 and pJB210 were introduced into umu $C36^{-}$ uvr $A6^{-}$ (TK610) strain and determined the protection effect and mutagenecity for UV and MMS. The protection effect and mutagenecity of umu $C36^{-}$ uvr $A6^{-}$ (TK610) were supressed by muc gene of the recombinant plasmids. The muc gene of pSL4 has higher effect than that of pKM101. The recombiant plasmid pJB210(inclued muc gene of pKM101) did not affect uv-mutagenesis in the $recA^{-}$ (JC2926) mutant.

• Natural Product Sciences
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• v.23 no.3
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• pp.201-207
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• 2017

Angelica decursiva has been utilised as remedy for controlling the airway inflammatory diseases in folk medicine. We investigated whether nodakenin, columbianadin, and umbelliferone isolated from the roots of Angelica decursiva inhibit the gene expression and production of MUC5AC mucin from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with nodakenin, columbianadin or umbelliferone for 30 min and then stimulated with epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) for 24 h. The MUC5AC mucin gene expression was measured by reverse transcription - polymerase chain reaction (RT-PCR). Production of MUC5AC mucin protein was measured by enzyme-linked immunosorbent assay (ELISA). The results were as follows: (1) Nodakenin did not affect the expression of MUC5AC mucin gene induced by EGF, PMA or $TNF-{\alpha}$. Columbianadin inhibited the expression of MUC5AC mucin gene induced by EGF or PMA. However, umbelliferone inhibited the expression of MUC5AC mucin gene induced by EGF, PMA or $TNF-{\alpha}$; (2) Nodakenin also did not affect the production of MUC5AC mucin protein induced by EGF, PMA or $TNF-{\alpha}$. Columbianadin inhibited the production of MUC5AC mucin protein induced by PMA. However, umbelliferone inhibited the production of MUC5AC mucin protein induced by EGF, PMA or $TNF-{\alpha}$. These results suggest that, among the three compounds investigated, umbelliferone only inhibits the gene expression and production of MUC5AC mucin stimulated by various inducers, by directly acting on airway epithelial cells, and the results might explain the traditional use of Angelica decursiva as remedy for diverse inflammatory pulmonary diseases.

• Natural Product Sciences
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• v.21 no.1
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• pp.59-65
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• 2015

In this study, we investigated whether cynaroside, cynarin and linarin derived from Chrysanthemum indicum L. affect the secretion, production and gene expression of MUC5AC mucin in airway epithelial cells. Confluent NCI-H292 cells were pretreated with cynaroside, cynarin or linarin for 30 min and then stimulated with PMA (phorbol 12-myristate 13-acetate) for 24 h. The MUC5AC mucin gene expression, mucin protein production and secretion were measured by RT-PCR and ELISA, respectively. Effect of linarin on EGF (epidermal growth factor) - or TNF-${\alpha}$ (tumor necrosis factor-${\alpha}$)-induced MUC5AC mucin gene expression and mucin protein production was also examined. The results were as follows: (1) Cynaroside and cynarin did not significantly affect PMA-induced MUC5AC mucin secretion from NCI-H292 cells. However, linarin decreased MUC5AC mucin secretion; (2) Cynaroside did not affect PMA-induced MUC5AC mucin production and gene expresion from NCI-H292 cells. However, cynarin and linarin inhibited the production and gene expression of MUC5AC mucin; (3) Linarin also inhibited the production and gene expression of MUC5AC mucin induced by EGF- or TNF-${\alpha}$ from NCI-H292 cells. These results suggest that linarin can regulate the gene expression, production and secretion of mucin, by directly acting on airway epithelial cells.

• Natural Product Sciences
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• v.23 no.1
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• pp.29-34
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• 2017

In this study, we investigated whether adenosine, adenine, uridine and homogentisic acid derived from Pinellia ternata affect the secretion, production and gene expression of MUC5AC mucin from airway epithelial cells. Confluent NCI-H292 cells were pretreated with adenosine, adenine, uridine or homogentisic acid for 30 min and then stimulated with PMA (phorbol 12-myristate 13-acetate) for 24 h. The MUC5AC mucin gene expression, mucin protein production and secretion were measured by RT-PCR and ELISA, respectively. The results were as follows: (1) Adenine and homogentisic acid decreased PMA-induced MUC5AC mucin gene expression, although adenosine and uridine did not affect the mucin gene expression; (2) Adenosine, adenine, uridine and homogentisic acid inhibited PMA-induced MUC5AC mucin production; (3) Homogentisic acid inhibited the secretion of MUC5AC mucin from NCI-H292 cells. These results suggest that, among the four compounds examined, homogentisic acid showed the regulatory effect on the steps of gene expression, production and secretion of mucin, by directly acting on airway epithelial cells.

• Tuberculosis and Respiratory Diseases
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• v.77 no.5
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• pp.203-208
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• 2014

Background: In this study, we investigated whether lobetyolin, lobetyol, and methyl linoleate derived from Codonopsis pilosula affect MUC5AC mucin secretion, production, and gene expression from airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with lobetyolin, lobetyol, or methyl linoleate for 30 minutes and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 hours. The MUC5AC mucin gene expression, and mucin protein production and secretion were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Results: Lobetyolin, lobetyol, and methyl linoleate inhibited the gene expression of MUC5AC mucin induced by PMA; lobetyolin did not affect PMA-induced MUC5AC mucin production. However, lobetyol and methyl linoleate inhibited the production of MUC5AC mucin; lobetyolin and lobetyol did not significantly affect PMA-induced MUC5AC mucin secretion from NCI-H292 cells. However, methyl linoleate decreased the MUC5AC mucin secretion. Conclusion: These results suggest that among the three compounds, methyl linoleate can regulate gene expression, production, and secretion of MUC5AC mucin by directly acting on the airway epithelial cells.

• The Journal of Internal Korean Medicine
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• v.29 no.3
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• pp.765-777
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• 2008

Objectives : In this study, the author tried to examine whether Gamijinhae-tang and Socheongryong-tang-ga-seokgo significantly affect both PMA-induced mucin production and MUC5AC gene expression from airway epithelial cells. Materials and Methods : Confluent NCI-H292 cells were pretreated for 30 min in the presence of JHT and STS and treated with PMA (10ng/ml), to assess the effects of the agents on PMA-induced mucin production by enzyme-linked immunosorbent assay (ELISA). Also, the effects of the agents on PMA-induced MUC5AC gene expression from the same cells were investigated. Possible cytotoxicities of the agent were assessed by examining the rate of survival and proliferation of NCI-H292 cells after treatment of agents during 48 hrs. Results : (1) JHT and STS did not show significant cytotoxicity to NCI-H292 cells. (2) JHT significantly decreased PMA-induced mucin production from NCI-H292 cells. However. STS did not affect mucin production. (3) JHT significantly inhibit the expression levels of PMA-induced MUC5AC gene in NCI-H292 cells. STS slightly decreased the expression levels of PMA-induced MUC5AC gene. Conclusion : These results suggest that JHT can not only affect the production of mucin but also affect the expression of the mucin gene, and this explains the traditional use of JHT in oriental medicine. The effects of JHT and STS with their components should be further investigated using animal experimental models that simulate pathophysiology of airway diseases through future studies.

• The Journal of Korean Medicine
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• v.29 no.4
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• pp.123-132
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• 2008

Objective: In this study, the author tried to investigate whether revised Seonbangpaedok-tang (SPT) and Sigyeongcheongpye-tang (SCT) significantly effects both PMA-induced mucin production and MUC5AC gene expression from airway epithelial cells. Objective: In this study, the author tried to investigate whether revised Seonbangpaedok-tang (SPT) and Sigyeongcheongpye-tang (SCT) significantly affects both PMA-induced mucin production and MUC5AC gene expression from airway epithelial cells. Materials and Methods: Confluent NCI-H292 cells were pretreated for 30 min in the presence of SPT and SCT and treated with PMA (10 ng/$m{\ell}$), to assess the effects of the agents on PMA-induced mucin production by enzyme-linked immunosorbent assay (ELISA). Also, the effects of the agents on PMA-induced MUC5AC gene expression from the same cells were investigated. Possible cytotoxicities of the agent were assessed by measuring the rate of survival and proliferation of NCI-H292 cells after treatment of agents during 48 hrs. Results: (1) SPT and SCT did not show significant cytotoxicity to NCI-H292 cells; (2) SPT significantly inhibitedthe expression levels of PMA-induced MUC5AC gene in NCI-H292 cells. SCT slightly decreased the expression levels of PMA-induced MUC5AC gene; (3) SPT significantly decreased PMA-induced mucin production from NCI-H292 cells. However, SCT did not affect mucin production. Conclusion: Theseresults suggest that SPT can not only affect the production of mucin but also the expression of the mucin gene and this explains the traditional use of SPT in oriental medicine. The effects of SPT and SCT with their components should be further investigated using animal experimental models that reflect pathophysiology of airway diseases via ongoing studies.

• Biomolecules & Therapeutics
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• v.18 no.3
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• pp.294-299
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• 2010

In this study, we tried to investigate whether platycodin D significantly affects MUC5AC mucin production and gene expression induced by epidermal growth factor (EGF), phorbol ester (PMA) and tumor necrosis factor-$\alpha$ (TNF-$\alpha$) from human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of platycodin D for 30 min and then stimulated with EGF, PMA and TNF-$\alpha$ for 24h, respectively. MUC5AC mucin gene expression and mucin protein production were measured by RT-PCR and ELISA. The results were as follows: (1) Platycodin D was found to inhibit the production of MUC5AC mucin protein induced by EGF, PMA, and TNF-$\alpha$, respectively. (2) It also inhibited the expression of MUC5AC mucin gene induced by the same inducers. These results suggest that platycodin D can regulate mucin gene expression and production of mucin protein, by directly acting on human airway epithelial cells.

• Molecules and Cells
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• v.46 no.11
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• pp.700-709
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• 2023

Mucus hyperproduction and hypersecretion are observed often in respiratory diseases. MUC8 is a glycoprotein synthesized by epithelial cells and generally expressed in the respiratory track. However, the physiological mechanism by which extracellular nucleotides induce MUC8 gene expression in human airway epithelial cells is unclear. Here, we show that UTP could induce MUC8 gene expression through P2Y2-PLCβ3-Ca²⁺ activation. Because the full-length cDNA sequence of MUC8 has not been identified, a specific siRNA-MUC8 was designed based on the partial cDNA sequence of MUC8. siRNA-MUC8 significantly increased TNF-α production and decreased IL-1Ra production, suggesting that MUC8 may downregulate UTP/P2Y2-induced airway inflammation. Interestingly, the PDZ peptide of ZO-1 protein strongly abolished UTP-induced TNF-α production and increased IL-1Ra production and MUC8 gene expression. In addition, the PDZ peptide dramatically increased the levels of UTP-induced ZO proteins and TEER (trans-epithelial electrical resistance). These results show that the anti-inflammatory mucin MUC8 may contribute to homeostasis, and the PDZ peptide can be a novel therapeutic candidate for UTP-induced airway inflammation.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.12
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• pp.7355-7358
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• 2013

Several lines of evidence support the notion that MUC1 is often aberrantly expressed in gastric cancer, and it is a ligand for Helicobacter pylori. Genetic variation in MUC1 gene may confer susceptibility to H. pylori infection and gastric cancer. We assessed the association of common polymorphisms in MUC1 gene with H. pylori infection and non-cardia gastric cancer using an LD-based tag SNP approach in north-western Chinese Han population. A total of four SNPs were successfully genotyped among 288 patients with non-cardia gastric cancer and 281 age- and sex-matched controls. None of the tested SNPs was associated with H. pylori infection. SNP rs9426886 was associated with a decreased risk of non-cardia gastric cancer, but lost significance after adjustment for multiple testing. Overall, our data indicated that common genetic variations in MUC1 gene might not make a major contribution to the risk of H. pylori infection and non-cardia gastric cancer in our studied population.