• 제목/요약/키워드: Mucins

검색결과 40건 처리시간 0.019초

Kaempferol Regulates the Expression of Airway MUC5AC Mucin Gene via IκBα-NF-κB p65 and p38-p44/42-Sp1 Signaling Pathways

  • Li, Xin;Jin, Fengri;Lee, Hyun Jae;Lee, Choong Jae
    • Biomolecules & Therapeutics
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    • 제29권3호
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    • pp.303-310
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    • 2021
  • In the present study, kaempferol, a flavonoidal natural compound found in Polygonati Rhizoma, was investigated for its potential effect on the gene expression and production of airway MUC5AC mucin. A human respiratory epithelial NCI-H292 cells was pretreated with kaempferol for 30 min and stimulated with epidermal growth factor (EGF) or phorbol 12-myristate 13-acetate (PMA), for the following 24 h. The effect on PMA-induced nuclear factor kappa B (NF-κB) signaling pathway or EGF-induced mitogen-activated protein kinase (MAPK) signaling pathway was investigated. Kaempferol suppressed the production and gene expression of MUC5AC mucins, induced by PMA through the inhibition of degradation of inhibitory kappa Bα (IκBα), and NF-κB p65 nuclear translocation. Also, kaempferol inhibited EGF-induced gene expression and production of MUC5AC mucin through regulating the phosphorylation of EGFR, phosphorylation of p38 MAPK and extracellular signal-regulated kinase (ERK) 1/2 (p44/42), and the nuclear expression of specificity protein-1 (Sp1). These results suggest kaempferol regulates the gene expression and production of mucin through regulation of NF-κB and MAPK signaling pathways, in human airway epithelial cells.

Pedunculated mucinous cystic neoplasm of the liver: a case report

  • Ha, Sang-Woo;Hwang, Shin;Han, Hyejin;Han, Song Ie;Hong, Seung-Mo
    • Journal of Yeungnam Medical Science
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    • 제39권3호
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    • pp.250-255
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    • 2022
  • In 2010, the World Health Organization classified mucin-producing bile duct tumors of the liver into two distinct entities; mucinous cystic neoplasm of the liver (MCN-L) and intraductal papillary mucinous neoplasm of the bile duct. We present the case of a patient with MCN-L having a uniquely pedunculated shape. A 32-year-old woman was referred to our institution with a diagnosis of biliary cystic neoplasm. She had undergone left salpingo-oophorectomy for ovarian cancer 15 years ago. Imaging studies showed an 8 cm-sized well defined, multiloculated cystic lesion suggesting a mucinous cystic neoplasm. The cystic mass was pedunculated at the liver capsule and pathologically diagnosed as MCN-L. The mass was resected with partial hepatectomy. The patient recovered uneventfully. She was discharged 7 days postoperatively. The patient has been doing well for 6 months after the operation. The patient will be followed up annually because of the favorable postresection prognosis of MCN-L.

Meclofenamate Suppresses MUC5AC Mucin Gene Expression by Regulating the NF-kB Signaling Pathway in Human Pulmonary Mucoepidermoid NCI-H292 Cells

  • Jiho Ryu;Kyung-il Kim;Rajib Hossain;Misoon Lee;Jin Tae Hong;Hyun Jae Lee;Choong Jae Lee
    • Biomolecules & Therapeutics
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    • 제31권3호
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    • pp.306-311
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    • 2023
  • The current study aimed to reveal the potential effect of meclofenamate, a nonsteroidal anti-inflammatory drug, on the gene expression of airway MUC5AC mucin. Human pulmonary mucoepidermoid NCI-H292 cells were pretreated with meclofenamate for 30 min and stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h. Thereafter, the effect of meclofenamate on the PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was assessed. Meclofenamate inhibited glycoprotein production and mRNA expression of MUC5AC mucins induced by PMA by inhibiting the degradation of inhibitory kappa Bα (IkBα) and NF-kB p65 nuclear translocation. These results suggest meclofenamate suppresses mucin gene expression by regulating NF-kB signaling pathway in human pulmonary epithelial cells.

Effect of Chrysin on Gene Expression and Production of MUC5AC Mucin from Cultured Airway Epithelial Cells

  • Shin, Hyun-Dae;Lee, Hyun Jae;Sikder, Asaduzzaman Md.;Park, Su Hyun;Ryu, Jiho;Hong, Jang-Hee;Kim, Ju-Ock;Seok, Jeong Ho;Lee, Choong Jae
    • Tuberculosis and Respiratory Diseases
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    • 제73권4호
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    • pp.204-209
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    • 2012
  • Background: We investigated whether chrysin affected MUC5AC mucin production and gene expression induced by phorbol ester (phorbol 12-myristate 13-acetate, PMA) or epidermal growth factor (EGF) from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with varying concentrations of chrysin for 30 minutes, and were then stimulated with PMA and EGF for 24 hours, respectively. MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Results: Concentrations of $10{\mu}M$ and $100{\mu}M$ chrysin were found to inhibit the production of MUC5AC mucin protein induced by PMA; A concentration of $100{\mu}M$ chrysin also inhibited the production of MUC5AC mucin protein induced by EGF; $100{\mu}M$ chrysin inhibited the expression of MUC5AC mucin gene induced by PMA or EGF. The cytotoxicity of chrysin was checked by lactate dehydrogenase assay, and there was no cytotoxic effect observed for chrysin. Conclusion: These results suggest that chrysin can inhibit mucin gene expression and the production of mucin protein by directly acting on airway epithelial cells.

Mometasone Furoate Suppresses PMA-Induced MUC-5AC and MUC-2 Production in Human Airway Epithelial Cells

  • Poachanukoon, Orapan;Koontongkaew, Sittichai;Monthanapisut, Paopanga;Pattanacharoenchai, Napaporn
    • Tuberculosis and Respiratory Diseases
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    • 제80권1호
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    • pp.60-68
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    • 2017
  • Background: Mucus hypersecretion from airway epithelium is a characteristic feature of airway inflammatory diseases. Tumor necrosis factor ${\alpha}$ (TNF-${\alpha}$) regulates mucin synthesis. Glucocorticoids including mometasone fuorate (MF) have been used to attenuate airway inflammation. However, effects of MF on mucin production have not been reported. Methods: Effects of MF and budesonide (BUD) on the phorbol-12-myristate-13-acetate (PMA)-induction of mucin and TNF-${\alpha}$ in human airway epithelial cells (NCI-H292) were investigated in the present study. Confluent NCI-H292 cells were pretreated with PMA (200 nM) for 2 hours. Subsequently, the cells were stimulated with MF (1-500 ng/mL) or BUD (21.5 ng/mL) for 8 hours. Dexamethasone ($1{\mu}g/mL$) was used as the positive control. Real-time polymerase chain reaction was used to determine MUC2 and MUC5AC mRNA levels. The level of total mucin, MUC2, MUC5AC, and TNF-${\alpha}$ in culture supernatants were measured using enzyme-linked immunosorbent assay. Results: MF and BUD significantly suppressed MUC2 and MUC5AC gene expression in PMA-stimulated NCI-H292 cells. The inhibitory effects of the two steroid drugs were also observed in the production of total mucin, MUC2 and MUC5AC proteins, and TNF-${\alpha}$. Conclusion: Our findings demonstrated that MF and BUD attenuated mucin and TNF-${\alpha}$ production in PMA-induced human airway epithelial cells.

Tilianin Inhibits MUC5AC Expression Mediated Via Down-Regulation of EGFR-MEK-ERK-Sp1 Signaling Pathway in NCI-H292 Human Airway Cells

  • Song, Won-Yong;Song, Yong-Seok;Ryu, Hyung Won;Oh, Sei-Ryang;Hong, JinTae;Yoon, Do-Young
    • Journal of Microbiology and Biotechnology
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    • 제27권1호
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    • pp.49-56
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    • 2017
  • In the human airway, mucus exists to protect the respiratory system as a primary barrier of the innate immune system. However, hyperexpressed mucus limits airflow, resulting in a decrease of lung function. Among more than 20 mucin family members, MUC5AC and MUC5B are major glycoproteins in human airway mucus. The epidermal growth factor receptor (EGFR) signaling pathway is one of the mechanisms of these mucins expression and specificity protein-1 (Sp1) transcription factor is the downstream signal of this pathway, playing pivotal roles in mucin expression. Even though there are some drugs for treating mucus hypersecretion, no drug has proven effects on humans. We found that the flavonoid tilianin regulated MUC5AC expression and also inhibited Sp1 phosphorylation. In this study, we investigated how tilianin would modulate EGFR signaling and regulate mucin production. In conclusion, tilianin inhibited MUC5AC expression mediated via modulating the EGFR-MEK-ERK-Sp1 signaling pathway in NCI-H292 human airway epithelial cells. This study may provide the basis for the novel treatment of mucus hypersecretion.

돌마자 Microphysogobio yaluensis(Cypriniformes, Cyprinidae) 후각기관의 구조 및 조직학적 특성 연구 (Structure and Histological Characters of the Olfactory Organ in Korean Endemic Fish, Microphysogobio yaluensis (Cypriniformes, Cyprinidae))

  • 김현태;이용주;김형수;박종영
    • 한국어류학회지
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    • 제30권3호
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    • pp.161-166
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    • 2018
  • 한국 고유종 돌마자 Microphysogobio yaluensis의 후각기관과 서식처 및 생태와의 연관성을 알아보기 위해 실체 현미경과 광학현미경을 이용하여 구조 및 조직학적 특징을 조사하였다. 후각기관은 외부적으로 전비공, 후비공 그리고 비경계판으로 구성되어 있으며, 내부는 22~24개의 후판들과 비선으로 구성되었다. 후판은 감각상피와 비감각상피로 이루어져 있는데, 감각상피는 후감각신경, 지지세포, 기저세포들로 구성되었으며, 비감각상피는 층상상피세포, 비감각섬모세포, 산성과 중성을 갖는 황점액소의 점액세포들로 구성되어 있다. 이러한 후각기관들의 특징들은 돌마자의 높은 후각능력과 의존성 그리고 서식처 환경에 밀접한 관계가 있을 것으로 생각되며 분류학적 연구에도 활용될 수 있을 것으로 생각된다.

Effects of Lobetyolin, Lobetyol and Methyl linoleate on Secretion, Production and Gene Expression of MUC5AC Mucin from Airway Epithelial Cells

  • Yoon, Yong Pill;Ryu, Jiho;Park, Su Hyun;Lee, Hyun Jae;Lee, Seungho;Lee, Sang Kook;Kim, Ju-Ock;Hong, Jang-Hee;Seok, Jeong Ho;Lee, Choong Jae
    • Tuberculosis and Respiratory Diseases
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    • 제77권5호
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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.

Apigenin and Wogonin Regulate Epidermal Growth Factor Receptor Signaling Pathway Involved in MUC5AC Mucin Gene Expression and Production from Cultured Airway Epithelial Cells

  • Sikder, Md. Asaduzzaman;Lee, Hyun Jae;Ryu, Jiho;Park, Su Hyun;Kim, Ju-Ock;Hong, Jang-Hee;Seok, Jeong Ho;Lee, Choong Jae
    • Tuberculosis and Respiratory Diseases
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    • 제76권3호
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    • pp.120-126
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    • 2014
  • Background: We investigated whether wogonin and apigenin significantly affect the epidermal growth factor receptor (EGFR) signaling pathway involved in MUC5AC mucin gene expression, and production from cultured airway epithelial cells; this was based on our previous report that apigenin and wogonin suppressed MUC5AC mucin gene expression and production from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with wogonin or apigenin for 15 minutes or 24 hours and then stimulated with epidermal growth factor (EGF) for 24 hours or the indicated periods. Results: We found that incubation of NCI-H292 cells with wogonin or apigenin inhibited the phosphorylation of EGFR. The downstream signals of EGFR such as phosphorylation of MEK1/2 and ERK1/2 were also inhibited by wogonin or apigenin. Conclusion: The results suggest that wogonin and apigenin inhibits EGFR signaling pathway, which may explain how they inhibit MUC5AC mucin gene expression and production induced by EGF.

Evaluation of host and bacterial gene modulation during Lawsonia intracellularis infection in immunocompetent C57BL/6 mouse model

  • Kirthika, Perumalraja;Park, Sungwoo;Jawalagatti, Vijayakumar;Lee, John Hwa
    • Journal of Veterinary Science
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    • 제23권3호
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    • pp.41.1-41.15
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    • 2022
  • Background: Proliferative enteritis caused by Lawsonia intracellularis undermines the economic stability of the swine industry worldwide. The development of cost-effective animal models to study the pathophysiology of the disease will help develop strategies to counter this bacterium. Objectives: This study focused on establishing a model of gastrointestinal (GI) infection of L. intracellularis in C57BL/6 mice to evaluate the disease progression and lesions of proliferative enteropathy (PE) in murine GI tissue. Methods: We assessed the murine mucosal and cell-mediated immune responses generated in response to inoculation with L. intracellularis. Results: The mice developed characteristic lesions of the disease and shed L. intracellularis in the feces following oral inoculation with 5 × 107 bacteria. An increase in L. intracellularis 16s rRNA and groEL copies in the intestine of infected mice indicated intestinal dissemination of the bacteria. The C57BL/6 mice appeared capable of modulating humoral and cell-mediated immune responses to L. intracellularis infection. Notably, the expression of genes for the vitamin B12 receptor and for secreted and membrane-bound mucins were downregulated in L. intracellularis -infected mice. Furthermore, L. intracellularis colonization of the mouse intestine was confirmed by the immunohistochemistry and western blot analyses. Conclusions: This is the first study demonstrating the contributions of bacterial chaperonin and host nutrient genes to PE using an immunocompetent mouse model. This mouse infection model may serve as a platform from which to study L. intracellularis infection and develop potential vaccination and therapeutic strategies to treat PE.