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  • 1995-1999  (2)
  • Airway epithelial cell  (1)
  • Calcium efflux  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Ozone exposure suppresses epithelium-dependent relaxation in feline airway (1995)
    Springer
    Lung 173 (1995), S. 47-56 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00167600
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Senescence marker protein-30 (SMP30) enhances the calcium efflux from renal tubular epithelial cells (1999)
    Springer
    Clinical and experimental nephrology 3 (1999), S. 261-267 
    Details
    ISSN: 1437-7799
    Keywords: Key words SMP30 ; Calcium efflux ; Tubular epithelia ; Calcium pump ; Calmodulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background. Senescence marker protein-30 (SMP30), a calcium binding protein, is preferentially expressed in the renal proximal tubules and hepatocytes and is presumed to play a role in Ca2+ homeostasis. Methods. To explore its physiological functions in the tubular cells, we investigated the effect of SMP30 on Ca2+ efflux via the ATP-dependent plasma membrane calcium pump. LLC-PK1 cells were stably transfected with a cDNA encoding SMP30, and the established transfectants were subjected to ATP responses. Results. Overexpression of SMP30 significantly increased Ca2+ efflux under both basal and ATP-stimulated conditions. Inhibition of calmodulin by trifluoperazine abrogated the enhanced Ca2+ efflux, suggesting that SMP30 activated the calmodulin-dependent Ca2+ pump. It is known that Ca2+ superfluous influx induces cellular injury. Compared with mock-transfected cells, LLC-PK1 cells expressing SMP30 showed resistance to cellular death triggered by Ca2+ superfluous influx. Conclusion. These results suggest the possibility that, in renal tubular cells, endogenous SMP30 participates in Ca2+ efflux via activating the calmodulin-dependent Ca2+ pump and thereby confers resistance of the cells against injury caused by high intracellular Ca2+ concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s101570050045
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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