Negative regulation of angiotensinogen gene expression by glucocorticoids in fetal sheep liver

Ann Louise Olson; Jean E Robillard; C Thomas Kisker; Bruce A Smith; Stanley Perlman

doi:10.1203/00006450-199109000-00011

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Negative regulation of angiotensinogen gene expression by glucocorticoids in fetal sheep liver

Journal article

Open access

Peer reviewed

Negative regulation of angiotensinogen gene expression by glucocorticoids in fetal sheep liver

Ann Louise Olson, Jean E Robillard, C Thomas Kisker, Bruce A Smith and Stanley Perlman

Pediatric research, Vol.30(3), pp.256-260

09/1991

DOI: 10.1203/00006450-199109000-00011

PMID: 1945565

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Abstract

The effect of glucocorticoids in regulating liver angiotensinogen gene expression was studied in chronically instrumented fetal sheep during the last trimester of gestation and was compared with the expression of other hepatic genes (prothrombin, factor IX, and albumin). Four sets of twins were studied at 118 d of gestation, and three sets were studied at 138 d of gestation (term, 145 d). One of each set of twins was infused intraperitoneally with cortisol (5 mumol.mL-1.h-1) for 48 h, whereas the other twin received the same volume (1 mL/h) of normal saline. Plasma cortisol concentration increased from 0.32 +/- 0.12 and 2.7 +/- 0.12 nmol/100 mL to 44.2 +/- 20.0 and 37.7 +/- 8.2 nmol/100 mL in 118- and 138-d fetuses, respectively, during the cortisol infusion; no changes were observed in fetuses infused with saline alone. At the end of the infusion period, the animals were anesthetized, the fetal liver was removed, and total cellular RNA was isolated and probed for angiotensinogen, prothrombin, factor IX, and albumin. The results demonstrated that cortisol infusion decreased angiotensinogen mRNA by 61% in 138-d fetuses and albumin mRNA expression by 2.4-fold in 118-d fetuses and by 3.4-fold in 138-d fetuses. On the other hand, cortisol had no effect on fetal factor IX gene expression but increased prothrombin mRNA levels by 65% in 118-d fetuses and 62% in 138-d fetuses. Taken together, our results suggest that, during fetal life, angiotensinogen gene expression is negatively regulated by glucocorticoids. This effect is not universal because cortisol increases fetal prothrombin gene expression.

Pregnancy

Liver - metabolism

RNA, Messenger - genetics

Fetus - metabolism

RNA, Messenger - metabolism

Gestational Age

Fetus - drug effects

Gene Expression Regulation - drug effects

Angiotensinogen - genetics

Animals

Liver - drug effects

Female

Sheep

Hydrocortisone - pharmacology

Details

Title: Subtitle: Negative regulation of angiotensinogen gene expression by glucocorticoids in fetal sheep liver
Creators: Ann Louise Olson - Department of Pediatrics, University of Iowa, Iowa City 52242
Jean E Robillard
C Thomas Kisker
Bruce A Smith
Stanley Perlman
Resource Type: Journal article
Publication Details: Pediatric research, Vol.30(3), pp.256-260
DOI: 10.1203/00006450-199109000-00011
PMID: 1945565
NLM abbreviation: Pediatr Res
ISSN: 0031-3998
eISSN: 1530-0447
Publisher: United States
Grant note: HD20576 / NICHD NIH HHS HL35600 / NHLBI NIH HHS DK38302 / NIDDK NIH HHS
Language: English
Date published: 09/1991
Academic Unit: Molecular Physiology and Biophysics; Microbiology and Immunology; Nephrology, Dialysis and Transplantation; Stead Family Department of Pediatrics; Iowa Neuroscience Institute; Medicine Administration; Infectious Disease (Pediatrics)
Record Identifier: 9983777470502771

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