Dexamethasone Enhances Surfactant Protein Gene Expression in Streptozotocin-Induced Immature Rat Lungs

Rayani, Hamid H.; Warshaw, Joseph B.; Floros, Joanna

doi:10.1203/00006450-199512000-00008

Cited by 4 publications

(1 citation statement)

References 51 publications

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“…We investigated whether therapeutic agents known to enhance terminal lung maturation and accelerate surfactant production could reverse the delaying effects of PFOS and therefore rescue the pups from respiratory distress. Dexamethasone is a synthetic glucocorticoid shown to accelerate lung maturation in lungs of normal rodents as well as pups with nitrofen‐induced congenital diaphragmatic hernia (CDH) or streptozotocin‐induced diabetes (Kauffman, 1977; Rotenberg and Gewolb, 1993; Rayani et al, 1995; Losty et al, 1996). Additionally, we utilized retinyl palmitate, a vitamin A derivative.…”

Section: Discussionmentioning

confidence: 99%

Effects of prenatal perfluorooctane sulfonate (PFOS) exposure on lung maturation in the perinatal rat

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Effects of prenatal perfluorooctane sulfonate (PFOS) exposure on lung maturation in the perinatal rat

et al. 2005

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GLUCOSE DECREASES STEADY STATE mRNA CONTENT OF HYDROPHOBIC SURFACTANT PROTEINS B AND C IN FETAL RAT LUNG EXPLANTS

Rayani

Gewolb

Floros³

1999

Experimental Lung Research

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The streptozotocin-induced diabetic (STZ-DB) rat model is associated with fetal hyperglycemia, but with low to normal plasma insulin concentration. Because surfactant protein (SP) mRNA content in fetal rat lung is decreased in STZ-DB pregnancy, we investigated the effect of increasing concentrations of glucose on SP gene expression in lung organ cultures. SP mRNA content (SP-A, SP-B, SP-C) was assessed by Northern blot analysis in fetal day 20 lung explants (term = 22 days) cultured for 44 hours in medium containing 10, 25, 50, or 100 mM glucose. Our findings were (1) No consistent alteration in SP-A mRNA content was observed at different glucose concentrations (P > .05); (2) SP-B and SP-C mRNA content were reduced in a dose-dependent manner when glucose concentration was increased from 10 mM to 100 mM. The mRNA content, compared to 10 mM glucose, decreased to 50-60% at 25 mM glucose, to 20-25% at 50 mM glucose, and to lower than 10% at 100 mM glucose (P < .01). These findings indicate that the decrease in SP-B and SP-C mRNA in fetuses of STZ-DB rats may be, in part, due to a direct effect of hyperglycemia, whereas the decrease in SP-A mRNA content in STZ-DB rats appears to be due to other effects of diabetes in pregnancy.

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Fetal Lung mRNA Levels of Hox Genes Are Differentially Altered by Maternal Diabetes and Butyrate in Rats

et al. 1998

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Diabetes is known to be associated with delayed lung development in humans and in experimental animals. This includes delayed expression of surfactant apoproteins. An important component of the metabolic abnormalities in diabetes is elevated levels of analogs of butyric acid, and the effects of diabetes on surfactant apoproteins can be reproduced by exposure of fetal rat lung explants to butyrate. Dexamethasone has the opposite effects on lung development. In humans, antenatal exposure to dexamethasone results in a lower incidence of RDS, whereas in experimental animals, dexamethasone increases the expression of surfactant apoproteins. A subset of Hox genes are expressed in developing lung, and their level of expression decreases with advancing gestation. We hypothesized that: 1) lungs of fetuses of rats with streptozotocin-induced diabetes would have altered levels of expression of Hox genes, 2) the effect would be mediated in part through elevated levels of butyrate, and 3) dexamethasone would reverse the effect. We tested our hypotheses in vivo using fetuses from streptozotocin-treated rats and in vitro by treating lung explants from normal rats with sodium butyrate. Streptozotocin treatment increased expression of Hoxb-5 at 18 d of gestation, but did not affect Hoxa-5 expression. This was associated with a 20-fold increase in alpha-aminobutyrate levels. Dexamethasone tended to reverse this effect. In contrast, butyrate treatment of explants decreased the expression of Hoxa-5 and Hoxb-5. We conclude that diabetes alters expression of Hox genes, but that the effect of butyrate on lung development, and in particular on surfactant apoprotein expression, is independent of its effects on Hox genes.

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Dexamethasone Enhances Surfactant Protein Gene Expression in Streptozotocin-Induced Immature Rat Lungs

Cited by 4 publications

References 51 publications

Effects of prenatal perfluorooctane sulfonate (PFOS) exposure on lung maturation in the perinatal rat

Effects of prenatal perfluorooctane sulfonate (PFOS) exposure on lung maturation in the perinatal rat

GLUCOSE DECREASES STEADY STATE mRNA CONTENT OF HYDROPHOBIC SURFACTANT PROTEINS B AND C IN FETAL RAT LUNG EXPLANTS

Fetal Lung mRNA Levels of Hox Genes Are Differentially Altered by Maternal Diabetes and Butyrate in Rats

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