Transcriptional activation of mucin by
            <i>Pseudomonas aeruginosa</i>
            lipopolysaccharide in the pathogenesis of cystic fibrosis lung disease

Li, Jian Dong; Dohrman, Austin F.; Gallup, Marianne; Miyata, Susumu; Gum, James R.; Kim, Young S.; Nadel, Jay A.; Prince, Alice; Basbaum, Carol

doi:10.1073/pnas.94.3.967

Cited by 268 publications

(230 citation statements)

References 22 publications

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“…MUC2 is approximately 17 kb in size, with 48 exons, and the protein product is more than 5100 amino acids long (20). Its promoter region was the first of the mucins to be elucidated (21). MUC2 is expressed primarily in the small intestine and colon of the GI tract (22), but its mRNA has also been detected in the airways of the lungs (23).…”

Section: Muc2 Expression and Regulationmentioning

confidence: 99%

“…Studies of MUC2 in the GI tract and its expression during carcinogenesis reveal that promoter DNA methylation is a frequent mechanism that controls MUC2 expression (142,143). Previous data indicate that the sequence of the MUC2 promoter region approximately 343 bp upstream of the transcription start site contains elements regulating MUC2 expression (21,22). Recent results demonstrate that the methylation level of this region, comprising nine CpG sites, is related to MUC2 expression in colon cancer cells in vitro (143) and pancreatic cancer in vivo (142).…”

Section: Muc2: An Example Of An Epigenetically Controlled Mucin Genementioning

confidence: 99%

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Regulation of Airway Mucin Gene Expression

Thai

Loukoianov

Wachi

et al. 2008

Annu. Rev. Physiol.

192

223

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Mucins are important components that exert a variety of functions in cell-cell interaction, epidermal growth factor receptor signaling, and airways protection. In the conducting airways of the lungs, mucins are the major contributor to the viscoelastic property of mucous secretion, which is the major barrier to trapping inhaled microbial organism, particulates, and oxidative pollutants. The homeostasis of mucin production is an important feature in conducting airways for the maintenance of mucociliary function. Aberrant mucin secretion and accumulation in airway lumen are clinical hallmarks associated with various lung diseases, such as asthma, chronic obstructive pulmonary disease, cystic fibrosis, emphysema, and lung cancer. Among 20 known mucin genes identified, 11 of them have been verified at either the mRNA and/or protein level in airways. The regulation of mucin genes is complicated, as are the mediators and signaling pathways. This review summarizes the current view on the mediators, the signaling pathways, and the transcriptional units that are involved in the regulation of airway mucin gene expression. In addition, we also point out essential features of epigenetic mechanisms for the regulation of these genes.

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Section: Muc2 Expression and Regulationmentioning

confidence: 99%

Section: Muc2: An Example Of An Epigenetically Controlled Mucin Genementioning

confidence: 99%

Regulation of Airway Mucin Gene Expression

Thai

Loukoianov

Wachi

et al. 2008

Annu. Rev. Physiol.

192

223

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“…It also induced mucin secretion from guinea pig tracheal epithelial cells (Fischer et al, 1999). Based on these reports, we investigated whether berberine affects EGF-, PMA-or TNF-α-induced MUC5AC mucin gene expression and mucin production from NCI-H292 cells, a human pulmonary mucoepidermoid cell line which is frequently used for studying intracellular signaling pathways involved in airway mucin production (Li et al, 1997;Takeyama et al, 1999;Shao et al, 2003). As can be seen in Results, berberine inhibited the production of MUC5AC mucin protein induced by EGF, PMA and TNF-α, respectively.…”

Section: Discussionmentioning

confidence: 99%

Effect of Berberine on MUC5AC Mucin Gene Expression and Mucin Production from Human Airway Epithelial Cells

Sikder¹,

Lee²,

Lee³

et al. 2011

Biomolecules and Therapeutics

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We conducted this study to investigate whether berberine signifi cantly affects MUC5AC mucin gene expression and mucin production induced by epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-α (TNF-α) from human airway epithelial cells. Confl uent NCI-H292 cells were pretreated with varying concentrations of berberine for 30 min and then stimulated with EGF, PMA or TNF-α for 24 h. MUC5AC mucin gene expression and mucin production were measured by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Berberine was found to inhibit the expression of MUC5AC mucin gene induced by EGF, PMA or TNF-α. Berberine also inhibited the production of MUC5AC mucin protein stimulated by the same inducers. This result suggests that berberine can regulate the expression of mucin gene and production of mucin protein, by directly acting on human airway epithelial cells. Abstractber of reports, Coptis japonica Makino and its components, berberine, have been used to control airway allergic or infl ammatory diseases and reported to have anti-infl ammatory and anti-cancer effects (Yoo et al., 2008;Sun et al., 2009;Tang et al., 2009). On the other hand, it was previously reported that berberine stimulated basal mucin release from airway goblet cells, by our group . However, to the best of our knowledge, there are no reports about the effect of berberine on MUC5AC mucin gene expression and mucin production induced by epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA) or tumor necrosis factor-α (TNF-α), from human airway epithelial cells. Therefore, in this study, we investigated whether berberine affects the expression of MUC5AC mucin gene and the production of mucin protein induced by EGF, PMA or TNF-α, from the NCI-H292 human pulmonary mucoepidermoid cell line.

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“…Phorbol 12-myristate 13-acetate (PMA) is an inflammatory stimulant affecting gene transcription, cell growth and differentiation and induces MUC5AC gene expression in NCI-H292 cells (Park et al, 2002;Hewson et al, 2004). Based on these reports, we investigated whether baicalin, baicalein or schizandrin affect EGF-and PMA-induced MUC5AC mucin production by NCI-H292 cells, a human pulmonary mucoepidermoid cell line which is frequently used for studying intracellular signaling pathways involved in airway mucin production (Li et al, 1997;Takeyama et al, 1999;Shao et al, 2003). Results showed that baicalin, baicalein and schizandrin each inhibited the production of MUC5AC mucin protein induced by EGF and PMA ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of Baicalin, Baicalein and Schizandrin on Airway Mucin Production Induced by Epidermal Growth Factor and Phorbol Ester

Lee¹,

Lee²,

Kim³

et al. 2010

Biomolecules and Therapeutics

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-We conducted this study to investigate whether baicalin, baicalein or schizandrin significantly affect MUC5AC mucin production induced by epidermal growth factor (EGF) or phorbol ester (PMA) in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with varying concentrations of baicalin, baicalein or schizandrin for 30 min and then stimulated with EGF or PMA for 24 h, respectively. MUC5AC mucin protein production was measured by ELISA. The results were as follows: (1) Baicalin was found to inhibit the production of MUC5AC mucin protein induced by both EGF and PMA. (2) Baicalein, the aglycone of baicalin, also inhibited MUC5AC mucin production. (3) Schizandrin, derived from Schizandrae Fructus, inhibited MUC5AC mucin production by the same inducers. These results suggest that baicalin, baicalein and schizandrin can regulate the production of mucin protein by directly acting on human airway epithelial cells.

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Transcriptional activation of mucin by Pseudomonas aeruginosa lipopolysaccharide in the pathogenesis of cystic fibrosis lung disease

Cited by 268 publications

References 22 publications

Regulation of Airway Mucin Gene Expression

Regulation of Airway Mucin Gene Expression

Effect of Berberine on MUC5AC Mucin Gene Expression and Mucin Production from Human Airway Epithelial Cells

Effects of Baicalin, Baicalein and Schizandrin on Airway Mucin Production Induced by Epidermal Growth Factor and Phorbol Ester

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