Dexamethasone has a biphasic effect on the c-Jun m-RNA expression in the fetal and adult rat lung, in vivo

Glucocorticoids are a very potent therapy for the treatment of asthma as well for lung maturation in the prematurely newborn animals and human. It has been demonstrated that glucocorticoid receptors antagonize the actions of inflammatory mediators through control of the specific DNA binding of the transcriptions factors c-Jun and c-Fos, and also decrease the mRNA and protein levels of these two transcription factors in a number of in vivo and in vitro studies. Additionally, glucocorticoids promote maturation of immature lungs, thereby increasing the production of surfactant proteins which are responsible for prevention of alveolar collapse. In the present study, the expression of c-Jun and the influence of dexamethasone on mRNA levels of c-Jun in different developmental stages in the rat lung, was examined. It was found that dexamethasone stimulated c-Jun expression throughout late gestational period, by similar to 50%. On day 16 postnatal, when developmental changes in the newborn lung have not been completed, dexamethasone also increased c-Jun expression by similar to 50%. Later, on postnatal day 35, when lung maturation and development has been completed, dexamethasone treatment resulted in lowered c-Jun expression, approximately 50%. During late fetal life and until postnatal day 16, c-Jun expression was gradually increased, indicating that c-Jun is needed to support lung development and normal function. On postnatal day 35, c-Jun mRNA levels showed a slight decrease. The biphasic effect of dexamethasone on c-Jun expression during rat lung development is of interest. It is possible that c-Jun participates in rat lung development through distinct mechanisms in different developmental stages