Physiological changes in maternal cortisol do not alter expression of growth-related genes in the ovine placenta.
OBJECTIVE
The aim of this study was to investigate the effect of cortisol on growth-related genes in the ovine placenta.


METHODS
Ewes carrying singleton pregnancies were operated on between 112 and 116 days of gestation (115 ± 0.4, term = 147 days) and randomly assigned into three groups: six control animals, five ewes that were administered cortisol by continuous intravenous infusion (1 mg/kg/day, high cortisol), and five ewes that were adrenalectomized and replaced with 0.5-0.6 mg cortisol/kg/day and 3 μg aldosterone/kg/day to produce cortisol concentrations equivalent to pre-pregnancy values (low cortisol). At necropsy (130 ± 0.2 days of gestation), placental tissue was frozen and stored at -80 °C for mRNA analysis.


METHODS
To assess potential molecular mechanisms by which cortisol alters placental structure and function and fetal growth.


RESULTS
Cortisol levels did not significantly affect 11β-hydroxysteroid dehydrogenase 1 and 2 enzymes, glucocorticoid receptor, mineralocorticoid receptor and angiotensin II receptor, type 1 (AT1R) expression levels. Gene expression levels of AT2R were increased in the high cortisol group for type B placentomes. There was little effect of cortisol on the insulin-like growth factor (IGF) axis. There was significantly more IGF-I mRNA in B versus A type and more IGFBP-2 mRNA in B and C type versus A type placentomes regardless of treatment (p < 0.05).


CONCLUSIONS
These data suggest that cortisol increases placental AT2R expression at high concentrations whereas it has little effect on the placental IGF axis.
Jensen
E C
EC
Department of Physiology, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand. e.knapp@auckland.ac.nz
Rochette
M
M
Bennet
L
L
Wood
C E
CE
Gunn
A J
AJ
Keller-Wood
M
M
D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000378:metabolism; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000378:metabolism; D000818:Animals; D005260:Female; D047109:Fetal Development; D015870:Gene Expression; D006854:Hydrocortisone / Q000378:metabolism*; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy / Q000378:metabolism*; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D018161:Receptors, Mineralocorticoid / Q000378:metabolism; D012756:Sheep; D013002:Somatomedins / Q000378:metabolism
D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D013002:Somatomedins; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2; D006854:Hydrocortisone