PMID- 12943992
OWN - NLM
STAT- MEDLINE
DCOM- 20040521
LR  - 20190813
IS  - 0303-7207 (Print)
IS  - 0303-7207 (Linking)
VI  - 206
IP  - 1-2
DP  - 2003 Aug 29
TI  - Adrenal TGFbeta1 mRNA levels fall during late gestation and are not regulated by 
      cortisol in the sheep fetus.
PG  - 85-91
AB  - During mammalian development there are periods when the fetal adrenal is either 
      relatively refractory or increasingly sensitive to trophic stimulation. This 
      pattern of regulation of adrenal growth and function ensures that the fetal 
      lungs, liver, brain and kidney are exposed in a programmed temporal sequence to 
      the genomic actions of circulating glucocorticoids. The factors which act to 
      maintain periods of adrenal quiescence are not known. In the present study we 
      have measured the level of messenger RNA (mRNA) expression of a putative 
      inhibitor of adrenal steroidogenesis, transforming growth factor beta 1 
      (TGFbeta1), and a key steroidogenic enzyme, cytochrome P450 17alpha hydroxylase 
      (CYP17), during periods of adrenal quiescence and activation in the sheep fetus. 
      We have also investigated the relative roles of the fetal hypothalamic-pituitary 
      axis and cortisol in the regulation of expression of adrenal TGFbeta1 and CYP17 
      mRNA during late gestation. Adrenal expression of TGFbeta1 was greatest at around 
      100 days gestation, at a time when the fetal sheep adrenal is relatively 
      refractory to trophic stimulation and there was an inverse relationship between 
      the expression of TGFbeta1 and CYP17 mRNA in the adrenal gland during the 
      peripartum period. Whilst disconnection of the fetal hypothalamic-pituitary 
      disconnection (HPD) axis resulted in a decrease in adrenal CYP 17 mRNA 
      expression, there was no effect of fetal HPD, with or without cortisol 
      replacement, on adrenal TGFbeta1 mRNA expression in late gestation. Thus TGFbeta1 
      may play a role in inhibiting adrenal steroidogenesis and ensuring that the 
      adrenal remains relatively refractory to trophic stimulation during mid 
      gestation. The maintenance of low adrenal TGFbeta1 expression during late 
      gestation is not dependent, however, on stimulation by the fetal 
      hypothalamic-pituitary axis.
FAU - Coulter, Catherine L
AU  - Coulter CL
AD  - Department of Physiology, Medical School Building, The University of Adelaide, 
      Adelaide, SA 5005, Australia. catherine.coulter@adelaide.edu.au
FAU - Salkeld, Mark D
AU  - Salkeld MD
FAU - McMillen, I Caroline
AU  - McMillen IC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta1)
RN  - EC 1.14.14.19 (Steroid 17-alpha-Hydroxylase)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Adrenal Cortex/*metabolism
MH  - Animals
MH  - Fetus
MH  - *Gene Expression Regulation, Developmental
MH  - *Gestational Age
MH  - Hydrocortisone/*physiology
MH  - Hypothalamus/physiology
MH  - Organ Size
MH  - Pituitary Gland/physiology
MH  - RNA, Messenger/analysis
MH  - Sheep
MH  - Steroid 17-alpha-Hydroxylase/genetics
MH  - Transforming Growth Factor beta/*genetics
MH  - Transforming Growth Factor beta1
EDAT- 2003/08/29 05:00
MHDA- 2004/05/22 05:00
CRDT- 2003/08/29 05:00
PHST- 2003/08/29 05:00 [pubmed]
PHST- 2004/05/22 05:00 [medline]
PHST- 2003/08/29 05:00 [entrez]
AID - S0303720703002144 [pii]
AID - 10.1016/s0303-7207(03)00214-4 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 2003 Aug 29;206(1-2):85-91. doi: 
      10.1016/s0303-7207(03)00214-4.