Disease relevance of Muc5ac

• Respiratory syncytial virus in allergic lung inflammation increases Muc5ac and gob-5 [1].
• NE induced Muc5ac mRNA and protein expression and goblet cell metaplasia on days 8, 11, and 14 [2].

High impact information on Muc5ac

• In addition, the STAT 1 KO-RSV mice showed induction of mucus production and expression of gob-5 and Muc5ac, conditions not present in any of the other 3 groups [3].
• IL-17, a cytokine that regulates Muc5ac expression, was expressed in the lungs of the STAT 1 KO-RSV mice, whereas lung levels of IL-17 were undetectable in the remaining groups [3].
• A subsequent search of the mouse genome database with the 3pmmuc5b-1 sequence identified two overlapping genomic clones (AC020817 and AC020794) that contained the sequence of both 3pmmuc5b-1 and the mouse Muc5ac gene [4].
• The expression of Muc5ac messenger RNA (mRNA) as well as glycoprotein was enhanced on Day 2, peaked on Day 4, and decreased on Day 7, whereas enhanced expression of mucin core 2 beta6 N-acetylglucosaminyltransferase (C2GnT)-M mRNA was not detected until Day 4 and peaked on Day 7 [5].
• Screening of a mouse stomach cDNA library with the anti-(deglycosylated MGM) antibody yielded partial clones containing a 48 bp tandem repeat and 768 bp of non-repetitive sequence [6].

Biological context of Muc5ac

• To further examine the role of macrophage accumulation in mucin gene expression, additional strains of mice (including a strain genetically deficient in macrophage metalloelastase) were exposed to acrolein for 3 wk, and Muc5ac mRNA levels and macrophage accumulation were measured [7].
• The MGM tandem repeat sequence bears no similarity to previously identified mucins [6].
• The MGM gene maps to a site on mouse chromosome 7 homologous to the location of a human secretory mucin gene cluster on human chromosome 11p15 [6].

Anatomical context of Muc5ac

• Muc5ac protein was expressed in some goblet transition and goblet cells [8].
• Lung Muc5ac mRNA was increased on days 12 and 19, and Muc5ac protein was detected in mucous granules and on the surface of the epithelium on day 19 [7].
• Monocyte inflammation augments acrolein-induced Muc5ac expression in mouse lung [7].
• Immunoreactivity of antibodies against deglycosylated MGM and against a synthetic MGM tandem repeat peptide was restricted to superficial mucous cells, antral glands and Brunner's glands in the pyloric-duodenal region [6].
• Bronchoalveolar lavage fluid (BALF) was collected and eosinophils were counted, and expression of Muc5ac mRNA and protein in lungs were detected by reverse transcription-polymerase chain reaction (RT-PCR) technology and immunohistochemical assay respectively [9].

Associations of Muc5ac with chemical compounds

• We hypothesized that this increased mucus was associated with mucosal expression of Muc5ac, a mucus gene expression in airways, and gob-5, a member of the Ca(2)(+)-activated chloride channel family [1].

Regulatory relationships of Muc5ac

• Effects of glucocorticoid on IL-13-induced Muc5ac expression in airways of mice [9].

Other interactions of Muc5ac

• The levels of Muc2 and Muc5ac mRNA were determined by RT-PCR, and the presence of Muc5ac protein was detected by immunohistochemistry [7].
• Despite eosinophils reduced (P<0.01), the number of mice with positive Muc5ac protein expression, expression of Muc5ac mRNA afterdexamethasone treatment didn't decreas significantly as compared with that of IL-13 group [9].

Analytical, diagnostic and therapeutic context of Muc5ac

• Although no goblet cells were observed, RT-PCR demonstrated the expression of Muc5ac RNA after approximately 22 days in culture [10].
• Our results showed that the number of mice, with positve Muc5ac protein expression, expression of Muc5ac mRNA and eosinophils in BALF after IL-13 treatment were all significantly higher than that of control group (all P<0.01) [9].

References