MUC5AC Expression (muc5ac + expression)

Distribution by Scientific Domains

Selected Abstracts

Quantitative analysis of MUC1 and MUC5AC mRNA in pancreatic juice for preoperative diagnosis of pancreatic cancer

Kenoki Ohuchida
Abstract Pancreatic juice is a promising type of diagnostic sample for pancreatic cancer, and members of the mucin (MUC) family are diagnostic candidates. To evaluate the utility of MUC family members as diagnostic markers, we measured MUC mRNA expression in pancreatic tissues and pancreatic juice obtained from patients with different pancreatic diseases as well as in pancreatic cancer cell lines by real-time PCR. Furthermore, to support the possibility of early diagnosis by quantification of MUC1 and MUC5AC, immunohistochemistry and microdissection-based quantitative analysis of mRNA were carried out. There was no significant correlation between MUC1 and MUC5AC expression in cell lines. When ,-actin was used as a reference gene, median MUC1 and MUC5AC mRNA expression levels were remarkably greater in tumoral tissues than in non-tumoral tissues, but median MUC4 and MUC6 mRNA expression levels were not. Receiver operating characteristic curve analysis showed that quantitative analysis of MUC1 and MUC5AC mRNA in pancreatic juice is better diagnostic modality than that of MUC4 and MUC6 mRNA. Immunohistochemistry showed that MUC1 and MUC5AC were highly expressed in invasive ductal carcinomas (IDC) and moderately expressed in high-grade pancreatic intraepithelial neoplasia (PanIN); no staining was observed in normal ducts. Analysis of cells isolated by microdissection showed stepwise upregulation of MUC1 and MUC5AC in the development of high-grade PanIN to IDC. Our results suggest that MUC1 and MUC5AC are upregulated stepwise in pancreatic carcinogenesis and that quantitative assessment of MUC1 and MUC5AC mRNA in pancreatic juice has high potential for preoperative diagnosis of pancreatic cancer. © 2005 Wiley-Liss, Inc. [source]

Muco-ciliary differentiation of nasal epithelial cells is decreased after wound healing in vitro

ALLERGY, Issue 8 2009
D. S. Lazard
Background:, Epithelial damage and modifications of cell differentiation are frequent in airway diseases with chronic inflammation, in which transforming growth factor-,1 (TGF-,1) plays an important role. The aim of this study was to evaluate the differentiation of human nasal epithelial cells (HNEC) after wound healing and the potential effects of TGF-,1. Methods:, Basal, mucus, and ciliated cells were characterized by cytokeratin-14, MUC5AC, and ,IV tubulin immunodetection, respectively. Their expression was evaluated in situ in nasal polyps and in an in vitro model of wound healing in primary cultures of HNEC after wound closure, under basal conditions and after TGF-,1 supplementation. Using RT-PCR, the effects of TGF-,1 on MUC5AC and DNAI1 genes, specifically transcribed in mucus and ciliated cells, were evaluated. Results:,In situ, high TGF-,1 expression was associated with low MUC5AC and ,IV tubulin expression. In vitro, under basal conditions, MUC5AC expression remained stable, cytokeratin-14 expression was strong and decreased with time, while ,IV tubulin expression increased. Transforming growth factor-,1 supplementation downregulated MUC5AC and ,IV tubulin expression as well as MUC5AC and DNAI1 transcripts. Conclusion:, After a wound, differentiation into mucus and ciliated cells was possible and partially inhibited in vitro by TGF-,1, a cytokine that may be involved in epithelial remodeling observed in chronic airway diseases. [source]

Mixed Nasal Mucus as a Model for Sinus Mucin Gene Expression Studies

FRCS, Mahmoud S. Ali MSc
Abstract Objective/Hypothesis It is necessary to obtain sinus mucus from the paranasal sinus cavities to study mucin gene expression occurring in the sinuses during chronic sinusitis. This requires an invasive procedure to access the sinus cavity. There are embryological as well as histological similarities between nasal and sinus epithelia; therefore, we postulated that the mucin expression in the secreted nasal and sinus mucins might be similar. Nasal mucus, which can be obtained easily, could then replace sinus mucus in these studies. Study Design Sinus and nasal mucus from six patients with chronic sinusitis were analyzed in this study. Methods High-molecular-weight glycoproteins (mucins) were isolated and purified by sequential density gradient centrifugation in caesium chloride (CsCl). Enzyme-linked immunosorbent assay was performed to identify the antigenic identity of these mucins. Results The MUC2, MUC5AC, and MUC5B mucin genes were all expressed in the nasal and sinus mucus secretions. Antigenic studies showed an inverse relationship between MUC2 and MUC5AC expression in nasal and sinus mucus secretions. The MUC5B gene was the major mucin gene expressed in sinus mucus but not in nasal mucus. Expression of MUC2 was significantly higher in sinus mucus. Expression of MUC5AC was different between nasal and sinus mucus. Conclusions Individual mucin expression in sinus and nasal mucus was markedly different. From this preliminary study, we conclude that nasal mucus is not a suitable substitute for sinus mucus in sinus mucin gene studies and that different pathological processes are taking place in nasal and sinus tissue in chronic sinusitis. [source]

Changes in the invasive and metastatic capacities of HT-29/M3 cells induced by the expression of fucosyltransferase 1

CANCER SCIENCE, Issue 7 2007
Raquel Mejías-Luque
Lewis antigens are terminal fucosylated oligosaccharides synthesized by the sequential action of several glycosyltransferases. The fucosyltransferases are the enzymes responsible for the addition of terminal fucose to precursor oligosaccharides attached to proteins or lipids. These oligosaccharides, defined as cell surface markers, have been implicated in different types of intercellular interactions and in adhesion and invasion processes. Transfection of HT-29/M3 colon cancer cells with the full length of human fucosyltransferase (FUT1), induces the synthesis of H type 2 and Lewis y antigens, associated with a decrease of sialyl-Lewis x. The capacity to develop primary tumors when cells were injected intrasplenically was similar in parental and FUT1-transfected cells, but the capacity to colonize the liver after spleen removal was significantly reduced in M3/FUT1 transfected cells. These results indicate that the expression of FUT1 induces changes in the metastatic capacity of HT-29/M3 colon cancer cells, as a consequence of the altered expression pattern of type 2 Lewis antigens. Also, an association between MUC5AC expression and the degree of gland differentiation in both primary splenic tumors and hepatic metastases was detected. (Cancer Sci 2007; 98: 1000,1005) [source]

Effect of pro-inflammatory stimuli on mucin expression and inhibition by secretory leucoprotease inhibitor

Siobhan Griffin
Summary Stimuli-induced expression of certain mucin genes has been demonstrated to occur as a result of ligand-dependent activation of the epidermal growth factor receptor (EGFR). In particular, MUC5AC expression can be induced by cigarette-smoke, neutrophil elastase and lipopolysaccharide (LPS) following activation of tumour necrosis factor ,-converting enzyme. We now show that a large of number of stimuli relevant to the cystic fibrosis lung , neutrophil elastase, LPS, Pam3Cys-Ser-(Lys)4 Hydrochloride (a lipopeptide analogue), CpG DNA (which mimics bacterial DNA) and cystic fibrosis bronchoalveolar lavage fluid , can activate MUC1 and 2 expression as well as MUC5AC expression in lung epithelial cells via an EGFR-dependent mechanism. In addition, we demonstrate that the immunomodulatory anti-protease, secretory leucoprotease inhibitor, can inhibit stimuli-induced MUC1, 2 and 5AC expression via a mechanism that is primarily dependent on the inhibition of transforming growth factor type alpha release. Therefore, mucin gene expression, induced by cystic fibrosis respiratory stimuli, can be inhibited by secretory leucoprotease inhibitor indicating its potential importance as an anti-mucin agent in cystic fibrosis and other chronic lung diseases characterized by mucus hypersecretion. [source]