Expression of Membrane-Bound Mucins in Human Nasal Mucosa

The formation of salivary glands entails the proliferation of epithelial cells from the stomatodeum into the underlying ectomesenchyme, culminating in a complex network of ducts and acinar bulbs. The extent to which mucins regulate this process is unknown, but they appear to mediate luminal space formation and maturation. Our aim was to examine mucin expression patterns during the morphogenesis of human salivary glands. Mucin expression -MUC1, 2, 3, 4, 5AC, 5B, 6, and 16 -was analyzed in specimens of developing human salivary glands, obtained from fetuses at 4-24 weeks' gestation, and fully developed salivary glands by immunohistochemistry. Expression patterns were analyzed qualitatively according to the development stage of the salivary glands. Mucins 1, 3, 4, 5B, and 16 were expressed during salivary gland development -being stronger in all ductal segments by the final phases of branching morphogenesis and in mature glands. Acinar cells were negative for most mucins, including MUC1 in mature salivary glands. Mucins 2, 5AC, and 6 were not expressed. Mucins MUC1, 3, 4, 5B, and 16 are expressed in developing human salivary glands and in mature glands, suggesting important roles in the maturation and maintenance of the ductal network.

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“…This protein is primarily expressed in human nasal mucosa, corneal epithelial cells, and ovarian cancers (Davies et al 2007;Woo et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Development of human minor salivary glands: expression of mucins according to stage of morphogenesis

et al. 2011

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“…When the cultures were confluent, the cells were exposed to the indicated concentrations of β-glucan. [11][12][13][14] The viability of normal nasal epithelial cells was determined by MTT assay (Sigma-Aldrich, St. Louis, MO). Passage 0 cells were only used to maintain the characteristics and purity of the epithelial cells in this study.…”

Section: Methodsmentioning

confidence: 99%

“…The primer sequences and conditions were used according to previously published protocols for MUC4, MUC16, MUC5AC, MUC5B, TLR2, and TLR4. 5,13,14 RNA integrity and the success of RT reactions were monitored by PCR amplification of the transcripts of the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene. PCR products were electrophoresed in 2% agarose gels, and visualized by staining with ethidium bromide and ultraviolet (UV) fluorescence.…”

Section: Methodsmentioning

confidence: 99%

Effect of β‐glucan on MUC4 and MUC5B expression in human airway epithelial cells

Kim

Bae

Song

et al. 2015

Int Forum Allergy Rhinol

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“…Each sample was reverse transcribed into cDNA using the GeneAmp RNA PCR Core Kit (Applied Biosystems). The primer sequences and conditions used were according to previously published protocols for MUC16, MUC8, MUC5B, MUC5AC, and MUC4 [11,12]. The PCR products were electrophoresed on a 2% agarose gel, stained with ethidium bromide, and visualized by UV fluorescence.…”

Section: Methodsmentioning

confidence: 99%

Visfatin induces MUC8 and MUC5B expression via p38 MAPK/ROS/NF-κB in human airway epithelial cells

et al. 2014

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BackgroundAmong a variety of inflammatory mediators, visfatin is a proinflammatory adipocytokine associated with inflammatory reactions in obesity, metabolic syndrome, chronic inflammatory disease, and autoimmune disease. However, the biological role of visfatin in secretion of major mucins in human airway epithelial cells has not been reported. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of visfatin on MUC8 and MUC5B expression in human airway epithelial cells.ResultsVisfatin significantly induced MUC8 and MUC5B expression. Visfatin significantly activated phosphorylation of p38 MAPK. Treatment with SB203580 (p38 MAPK inhibitor) and knockdown of p38 MAPK by siRNA significantly blocked visfatin-induced MUC8 and MUC5B expression.Visfatin significantly increased ROS formation. Treatment with SB203580 significantly attenuated visfatin-induced ROS formation. Treatment with NAC (ROS scavenger) and DPI (NADPH oxidase inhibitor) significantly attenuated visfatin-induced MUC8 and MUC5B expression. However, treatment with NAC and DPI did not attenuate visfatin-activated phosphorylation of p38 MAPK. Visfatin significantly activated the phosphorylation of NF-κB. Treatment with PDTC (NF-κB inhibitor) significantly attenuated visfatin-induced MUC8 and MUC5B expression.ConclusionsThese results suggest that visfatin induces MUC8 and MUC5B expression through p38 MAPK/ROS/NF-κB signaling pathway in human airway epithelial cells.

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Expression of Membrane-Bound Mucins in Human Nasal Mucosa

Abstract: Expression of MUC4 and MUC16 are regulated differently in nasal mucosa. Dexamethasone and PMA are potent mediators for the expression of MUC16 in nasal polyps.

Cited by 21 publications

References 20 publications

Development of human minor salivary glands: expression of mucins according to stage of morphogenesis

Development of human minor salivary glands: expression of mucins according to stage of morphogenesis

Effect of β‐glucan on MUC4 and MUC5B expression in human airway epithelial cells

Visfatin induces MUC8 and MUC5B expression via p38 MAPK/ROS/NF-κB in human airway epithelial cells

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