Abstract
Glucocorticoids produce most of their effects by inducing the synthesis of endogenous, phospholipase A2 inhibitory proteins, such as lipomodulin (J Biol Chem 256:7730). Glucocorticoids also increase the cellular numbers of β-AR in the lung (Bioch Biophys Res Commun 94:390), which may be the mechanism of the synergism between glucocorticoids and β-adrenergic agonists for increasing surfactant production, and of the sensitization of the lung to β-adrenergic bronchodilation. We studied the mechanism of the increase in β-AR by glucocorticoids in a human lung adenocarcinoma cell line (A549) frequently used as a model of alveolar type II cells. Cells were cultured to confluency in RPMI 164 medium containing 10% fetal calf serum. Cells were then incubated for a further 24 hours in serum-free Dulbecco MEM with or without 10 μM corticosterone, in the presence of 5 μl/ml of saline (S), a monoclonal antibody of lipomodulin (AB), or control ascites fluid (ASC). Cells detached in calcium-free medium were freeze-thawed, and β-AR binding was assayed using 125I-cyanopindolol. CORT increased β-AR/cell from 680 to 1460 in S and from 240 to 1650 in ASC (P < 0.05 for both), but CORT was ineffective in the presence of AB (450 vs 480 β-AR/cell). These findings suggest that glucocorticoids do not directly induce the synthesis of lung β-AR, but increase their numbers indirectly through the induction of the phospholipase inhibitory protein, lipomodulin.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Vermes-Kunos, I., Kunos, G., Birata, F. et al. 326 LIPOMODULIN ANTIBODY PREVENTS THE GLUCOCORTICOIDINDUCED INCREASE ON PULMONARY B-ADRENERGIC RECEPTORS (β-AR). Pediatr Res 19, 165 (1985). https://doi.org/10.1203/00006450-198504000-00356
Issue Date:
DOI: https://doi.org/10.1203/00006450-198504000-00356