Glucocorticoid Effects in Vivo

Ballard, Philip L.

doi:10.1007/978-3-642-82483-8_2

Hormones and Lung Maturation

1986

DOI: 10.1007/978-3-642-82483-8_2

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Glucocorticoid Effects in Vivo

Philip L. Ballard¹

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1993

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Cited by 10 publications

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“…It has been shown in intact animal models that maternally administered glucocorticoids increase fetal lung phospholipid synthesis and secretion and accelerate the morphological development of the fetal lung (Ballard, 1986). The induction of the surfactant-associated proteins in developing lung tissue is also hormonally regulated .…”

mentioning

confidence: 99%

Glucocorticoid regulation of surfactant‐associated proteins in rabbit fetal lung in vivo

1993

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The effects of a maternally administered synthetic glucocorticoid, betamethasone, on the levels of mRNA for the surfactant proteins SP-A, SP-B, and SP-C and on the levels of SP-A protein were investigated in day 27 gestational age rabbit fetal lung tissue. Betamethasone administration to the pregnant rabbit caused approximately a twofold increase in the fetal lung level of SP-A protein and a threefold increase in fetal lung SP-A mRNA levels when compared to levels in fetuses obtained from saline-treated or uninjected animals. SP-B mRNA was increased fourfold in fetal lung tissue obtained from glucocorticoid-treated pregnant does when compared to levels in fetuses of uninjected pregnant does. However, SP-B mRNA levels in fetal lung tissue from saline-injected controls were also significantly elevated, approximately twofold, when compared to fetal lung SP-B mRNA levels in the uninjected control condition. SP-C mRNA levels in lung tissue of fetuses from both saline-injected and betamethasone-injected pregnant does were increased similarly, approximately twofold, over SP-C mRNA levels in fetal lung tissue obtained from uninjected control does. These data are suggestive that betamethasone treatment increases fetal lung SP-A and SP-B mRNA levels and that maternal stress alone can increase the expression of SP-B and SP-C mRNA in rabbit fetal lung tissue. Using in situ hybridization, SP-A mRNA was shown to be present primarily in alveolar type II cells in fetuses of control and saline-injected does. However, SP-A mRNA was easily detected in both alveolar type II cells and bronchiolar epithelial cells of rabbit fetal lung tissue following maternal betamethasone treatment. In contrast, SP-B and SP-C mRNA were present only in alveolar type II cells of lung tissue obtained from fetuses of control, saline, or betamethasone-treated does. Thus maternal administration of glucocorticoids increased SP-A protein as well as SP-A and SP-B mRNA levels in rabbit fetal lung tissue. SP-A mRNA was localized to both alveolar type II cells and in smaller amounts in bronchiolar epithelial cells of rabbit fetal lung tissue. However, SP-B and SP-C mRNA were detected only in alveolar type II cells.

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Glucocorticoid regulation of surfactant‐associated proteins in rabbit fetal lung in vivo

1993

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Intraalveolar bubbles and bubble films I. Formation and development during the first 48 hours of extrauterine life in rabbits

1996

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Loss of glucocorticoid-dependent growth inhibition in transformed mouse lung cells

Johnson

Hanson

et al. 1996

Mol. Carcinog.

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Transformed A5 mouse lung cells were examined for mechanisms that may explain their loss of glucocorticoid-induced growth inhibition. These cells were compared to nontransformed C10 mouse lung cells, which retain this response. Southern blot analysis revealed no major differences in the amount or pattern of restriction fragments for the glucocorticoid receptor (GR) gene between the responsive and nonresponsive cells. Northern blot analysis demonstrated that both cell lines expressed GR mRNA at similar levels and that these mRNAs had similar relative stabilities. The mRNA from both cell lines was used for reverse transcription-polymerase chain reaction amplification and direct sequencing with primers for different regions of the GR cDNA. A conservative mutation previously shown not to affect receptor function was detected within the DNA-binding domain region of the GR from both cell lines. Because of the ability of the transcription factors for activator protein-1 to antagonize GR function, c-jun and c-fos mRNA levels were examined. A5 cells were found to have higher levels of c-jun mRNA than C10 cells both during active cell growth and after serum starvation. Stable transfection of the nonresponsive A5 cells with a rat GR expression vector (A5GR7) resulted in strong glucocorticoid-induced growth inhibition, demonstrating that these cells retain the ability to be growth inhibited by these steroids. The A5GR7 transfectants also had higher mouse mammary tumor virus (MMTV)-chloramphenicol acetyltransferase (CAT) activity than the parental A5 cells and lower levels of c-jun during active cell growth. Transient transfection of the C10 cells with c-jun expression vector strongly reduced glucocorticoid-inducible MMTV-CAT activity. These results suggest that the transformed A5 cells apparently contain functional GR but that the high level of c-jun mRNA expression (probably resulting from the activated Ki-ras allele in these cells) may antagonize their ability to respond to the growth-inhibitory signaling of glucocorticoids.

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Glucocorticoid Effects in Vivo

Cited by 10 publications

References 129 publications

Glucocorticoid regulation of surfactant‐associated proteins in rabbit fetal lung in vivo

Glucocorticoid regulation of surfactant‐associated proteins in rabbit fetal lung in vivo

Intraalveolar bubbles and bubble films I. Formation and development during the first 48 hours of extrauterine life in rabbits

Loss of glucocorticoid-dependent growth inhibition in transformed mouse lung cells

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