Expression of MUC5AC mRNA in the Goblet Cells of Human Nasal Mucosa

Kim, Chang Hoon; Song, Kyoung Seob; Kim, Sung Shik; Kim, Hyun Ung; Seong, Je Kyung; Yoon, Joo Heon

doi:10.1097/00005537-200012000-00026

Cited by 29 publications

(31 citation statements)

References 13 publications

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“…Accordingly, most studies on mucin genes have been focused on these two mucins. However, although MUC5AC is known to be expressed by most surface goblet cells, we found that only a portion of the goblet cells (11) expressed MUC5AC mRNA. This suggests that other mucin genes in addition to MUC5AC might be important for mucus hypersecretion.…”

contrasting

confidence: 67%

Induction of MUC8 Gene Expression by Interleukin-1β Is Mediated by a Sequential ERK MAPK/RSK1/CREB Cascade Pathway in Human Airway Epithelial Cells

Song

Seong

Chung

et al. 2003

Journal of Biological Chemistry

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Mucins are the major components of the mucus layer that covers and protects the respiratory, digestive, and reproductive tracts. Our previous studies showed that MUC8 gene expression was overexpressed in in vivo polyp epithelium in chronic sinusitis and was also increased by treatment with inflammatory mediators in an in vitro culture condition. However, the mechanisms by which the inflammatory mediators-induced MUC8 gene expression in normal nasal epithelial cells evolved remain unclear. We examined the mechanism by which the important proinflammatory mediator, interleukin (IL)-1␤, increases MUC8 gene expression levels. We found that pharmacologic and genetic inhibition of ERK MAPK pathway abolished IL-1␤-induced MUC8 gene expression in normal human nasal epithelial cells. Moreover, the overexpression of wide-type or of the dominant-negative mutant of p90 ribosomal S6 protein kinase 1 (RSK1) enhanced or suppressed, respectively, IL-1␤-induced MUC8 gene expression. RSK1 was found to directly phosphorylate cAMP-response element-binding protein (CREB), and this event led to the stimulation of subsequent CRE-mediated gene transcription. In conclusion, IL-1␤ was found to induce MUC8 gene expression via a sequential ERK/RSK1/CREB pathway in human airway epithelial cells.

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confidence: 67%

Induction of MUC8 Gene Expression by Interleukin-1β Is Mediated by a Sequential ERK MAPK/RSK1/CREB Cascade Pathway in Human Airway Epithelial Cells

Song

Seong

Chung

et al. 2003

Journal of Biological Chemistry

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“…In our group of 24 CRS cases, the expression of MUC5AC and MUC5B were much more higher than MUC1 and MUC2, which indicated MUC5AC and MUC5B are the dominant ones affecting the pathology of CRS. According to most literature, MUC5AC was mainly detected in goblet cells while MUC5B is located in submucosal glands [4,7,8]. Our data were in agreement with these results, meanwhile, our study also indicated MUC5AC was weakly expressed in submucosal glands, and MUC5B in goblet cells as well.…”

Section: Discussionsupporting

confidence: 92%

Increased expression of MUC5AC and MUC5B promoting bacterial biofilm formation in chronic rhinosinusitis patients

Mao¹,

Chen²,

Wang³

et al. 2015

Auris Nasus Larynx

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“…EGF-receptor activation may lead to an increase in mucin MUC5AC gene expression and goblet cell hyperplasia. MUC5AC expression is higher in nasal polyp epithelial cells than in nasal mucosa [44][45][46].…”

Section: Growth Factorsmentioning

confidence: 88%

Pathogenesis of nasal polyps: An update

Pawliczak

Lewandowska–Polak

Kowalski

2005

Curr Allergy Asthma Rep

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The cause of nasal polyp formation is still unknown. Genetic predisposition has been suggested, but there are scanty data to support such theories. Activated epithelial cells may be the major source of mediators inducing influx of inflammatory cells (mostly eosinophils) and proliferation and activation of fibroblasts leading to nasal polyp formation. Infectious agents (including viruses, bacteria, or fungi) may be potential primary factors activating nasal epithelial cells. Proinflammatory cytokines and growth factors play important roles in the persistence of mucosal inflammation associated with nasal polyps. Arachidonic acid metabolites seem to be particularly important in the pathogenesis of nasal polyps in patients with aspirin hypersensitivity rhinosinusitis/asthma syndrome.

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Expression of MUC5AC mRNA in the Goblet Cells of Human Nasal Mucosa

Cited by 29 publications

References 13 publications

Induction of MUC8 Gene Expression by Interleukin-1β Is Mediated by a Sequential ERK MAPK/RSK1/CREB Cascade Pathway in Human Airway Epithelial Cells

Induction of MUC8 Gene Expression by Interleukin-1β Is Mediated by a Sequential ERK MAPK/RSK1/CREB Cascade Pathway in Human Airway Epithelial Cells

Increased expression of MUC5AC and MUC5B promoting bacterial biofilm formation in chronic rhinosinusitis patients

Pathogenesis of nasal polyps: An update

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