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.
Department of Physiology, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand. e.knapp@auckland.ac.nz
E C
EC
Jensen
M
M
Rochette
L
L
Bennet
C E
CE
Wood
A J
AJ
Gunn
M
M
Keller-Wood
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