The Combined Effects of Insulin and Cortisol on Surfactant Protein mRNA Levels

Dekowski, Steven A.; Snyder, Jeanne M.

doi:10.1203/00006450-199510000-00007

Cited by 30 publications

(16 citation statements)

References 47 publications

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“…In vivo, induced diabetes in pregnant rats interferes with normal expression patterns of SP-A, SP-B and SP-C mRNA in the developing fetal lung. 89,90 Furthermore, increased insulin concentrations have been shown to decrease SP-A, SP-B and SP-D mRNA expression in mid-gestation human fetal lung explants 91 and inhibit Type II AEC differentiation in late gestation fetal rat lung explants. 92 Although it has been clearly demonstrated that increased plasma glucose and/or insulin concentrations are implicated in delayed maturation of the surfactant system, the underlying molecular mechanisms are unknown.…”

Section: Fetal Consequences Of Maternal Obesity and Gestational Diabementioning

confidence: 98%

Regulation of fetal lung development in response to maternal overnutrition

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McGillick

Orgeig

et al. 2013

Clin Exp Pharma Physio

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With the worldwide obesity epidemic, the proportion of women entering pregnancy overweight or obese has increased significantly in recent years. Babies born to obese women are at an increased risk of respiratory complications at birth and in childhood. In addition to maternal diabetes, there are a number of metabolic changes that the fetus of an overnourished mother experiences in utero that may modulate lung development and represent the mechanisms underlying the increased risk of respiratory complications. Herein we highlight a series of factors associated with the intrauterine environment of an overnourished mother that may impact on fetal lung development and lead to an increased risk of complications at birth or in postnatal life.

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Section: Fetal Consequences Of Maternal Obesity and Gestational Diabementioning

confidence: 98%

Regulation of fetal lung development in response to maternal overnutrition

Lock

McGillick

Orgeig

et al. 2013

Clin Exp Pharma Physio

View full text Add to dashboard Cite

show abstract

“…In human fetal lung explants, the synthetic glucocorticoid dexamethasone increases SP-A mRNA levels at low concentrations ( 10 nM), but decreases SP-A mRNA and protein levels at higher concentrations (100 nM) [10][11][12][13][14][15]. Moreover, the degree of inhibition of SP-A1 and SP-A2 expression varies in explant cultures [16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid inhibition of human SP-A1 promoter activity in NCI-H441 cells

Hoover

Thomas

Floros

1999

Biochemical Journal

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Glucocorticoids have complex effects on human surfactant protein (SP) SP-A1 and SP-A2 gene expression that occur at both transcriptional and post-transcriptional levels. In the lung adenocarcinoma cell line NCI-H441, dexamethasone causes a dose-dependent decrease in total SP-A mRNA levels and inhibits SP-A gene transcription. In this study, a deletional analysis of the SP-A1 promoter was performed in order to identify cisacting elements that mediate dexamethasone responsiveness in NCI-H441 cells. The region k32\j63 relative to the start of SP-A1 transcription mediated both basal promoter activity and dexamethasone repression of transcription. Removal of the

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“…In human fetal lung explants, GCs reduce SP-A gene expression in a time-and dose-dependent manner. At low concen-trations (Ͻ10 nM), GCs increase SP-A mRNA levels (5,14,28,39,43), and at high concentrations (100 nM), GCs decrease SP-A expression (26-28, 31, 43). In contrast, Dex at 1-100 nM has only an inhibitory effect on SP-A gene expression in the lung adenocarcinoma cell line NCI-H441 (50,52).…”

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confidence: 99%

Human SP-A 3′-UTR variants mediate differential gene expression in basal levels and in response to dexamethasone

Wang¹,

Guo²,

Floros

2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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Human surfactant protein A (SP-A) is encoded by two genes ( SP-A1, SP-A2), and each is identified with several alleles. SP-A is involved in normal lung function, innate immunity, inflammatory processes, and is regulated by glucocorticoids. We investigated the role of 3′-untranslated region (UTR) of 10 SP-A variants on gene expression using transient transfection of 3′-UTR constructs in the human lung adenocarcinoma cell line NCI-H441. We found: 1) both basal mRNA and protein levels of the reporter gene of SP-A 3′-UTR constructs are significantly ( P < 0.01) reduced compared with controls (vector pGL3 and surfactant protein B pGL3) and that differences exist among alleles; and 2) after dexamethasone (Dex) treatment (100 nM for 16 h), mRNA was reduced (31–51%). Seven alleles showed a significant decrease ( P < 0.05) in mRNA, and three did not. Reporter activity was also decreased, from 17% (1A1) to 38% (1A), with six alleles showing a significant decrease. The data indicate that the 3′-UTR of SP-As play a differential role in SP-A basal expression and in response to Dex. Therefore, a careful consideration of individual use of steroid treatment may be considered.

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The Combined Effects of Insulin and Cortisol on Surfactant Protein mRNA Levels

Cited by 30 publications

References 47 publications

Regulation of fetal lung development in response to maternal overnutrition

Regulation of fetal lung development in response to maternal overnutrition

Glucocorticoid inhibition of human SP-A1 promoter activity in NCI-H441 cells

Human SP-A 3′-UTR variants mediate differential gene expression in basal levels and in response to dexamethasone

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