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  • 1995-1999  (2)
  • Airway epithelial cell  (1)
  • Neurospora crassa
  • 1
    ISSN: 1432-1750
    Keywords: Airway hyperresponsiveness ; Ozone ; Airway epithelial cell ; Bronchiole ; Cat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the effect of exposure to ozone on the epithelium-dependent relaxation (EpDR) of bronchioles evoked by electrical field stimulation (EFS) in a feline model with hyperresponsive airways induced by exposure to ozone. Airway responsiveness was assessed by measuring the increases in total pulmonary resistance (RL) produced by aerosolized acetylcholine (ACh) in vivo. Airway responsiveness was also measured in vitro in dissected bronchiolar ring preparations. Exposure to ozone (3 ppm, 2 h) significantly increased the airway responsiveness in vivo. The concentration of ACh required increasing R L to 200% of the baseline value, decreased from 1.97 mg/ml (GSEM 1.94) to 0.12 mg/ml (GSEM 1.77, p 〈 0.01) after exposure to ozone. EFS evoked atropine-, guanethidine-, and tetrodotoxin-resistant relaxations in the control bronchiolar rings precontracted by 5-hydroxytryptamine. Such relaxation was significantly suppressed by the mechanical denudation of epithelium, confirming that it was epithelium dependent. The amplitude of EpDR was significantly suppressed in the animals exposed to ozone. These results suggest that EpDR is present in cats, and that its inhibition may contribute to the development of airway hyperresponsiveness.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1617-4623
    Keywords: Key wordslah-1 ; cpc-1 ; Laccase ; Cycloheximide-inducible genes ; Neurospora crassa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In Neurospora crassa, expression of the laccase gene is induced by treatment with the protein synthesis inhibitor cycloheximide (CHX). This expression is mediated by CPC1, which acts as a general transcriptional activator when mycelia are treated with CHX or starved for any one of the amino acids. A laccase-derepressed mutant, lah-1, shows pleiotropic deficiencies in growth, hyphal morphology, CHX sensitivity, and production of protoperithecia. Moreover, in the lah-1 mutant, transcript levels of CHX-inducible genes, including lacc, tub-2, tef-1, and amino acid biosynthetic genes such as cpc-1, trp-3, and arg-12, are increased without exposure to CHX. All of the defects exhibited in the lah-1 mutant are suppressed by a mutation in the cpc-1 locus. These findings suggest that the cpc-1 mutation is epistatic to the lah-1 mutation and that the pleiotropic defects in the lah-1 mutant are attributable to constitutive expression of CPC1. These conclusions are supported by a developmental Northern blot analysis of the CHX-inducible genes. Based on these results, the lah-1 gene product appears to regulate expression of the cpc-1 gene negatively. Expression of the CHX-inducible genes was induced by CHX treatment in the lah-1 cpc-1 mutant, as well as in the cpc-1 mutant. This observation indicates that LAH1 is not a component of CHX-responsive pathway itself.
    Type of Medium: Electronic Resource
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