In:
American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 273, No. 5 ( 1997-11-01), p. L1013-L1019
Abstract:
Airway epithelial cells (AEC) metabolize arachidonic acid (AA) to biologically active eicosanoids, which contribute to regulation of airway smooth muscle tone and inflammatory responses. Although in vivo the airways undergo cyclical stretching during ventilation, the effect of cyclic stretch on airway epithelial AA metabolism is unknown. In this study, cat and human AEC were grown on flexible membranes and were subjected to cyclic stretch using the Flexercell strain unit. Cyclic stretch downregulated synthesis of prostaglandin (PG) E 2 , PGI 2 , and thromboxane A 2 by both cell types in a frequency-dependent manner. The percent inhibition of prostanoid synthesis in both cell types ranged from 53 ± 7 to 75 ± 8% (SE; n = 4 and 5, respectively). Treatment of cat AEC with exogenous AA (10 μg/ml) had no effect on the stretch-induced inhibition of PGE 2 synthesis, whereas treatment with exogenous PGH 2 (10 μg/ml) overcame the stretch-induced decrease in PGE 2 production. These results indicate that stretch inhibits prostanoid synthesis by inactivating cyclooxygenase. When cells were pretreated with the antioxidants catalase (100 μg/ml, 150 U/ml) and N-acetylcysteine (1 mM), there was a partial recovery of eicosanoid production, suggesting that cyclic stretch-induced inactivation of cyclooxygenase is oxidant mediated. These results may have important implications for inflammatory diseases in which airway mechanics are altered.
Type of Medium:
Online Resource
ISSN:
1040-0605
,
1522-1504
DOI:
10.1152/ajplung.1997.273.5.L1013
Language:
English
Publisher:
American Physiological Society
Publication Date:
1997
detail.hit.zdb_id:
1477300-4
SSG:
12
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