PMID- 8200959
OWN - NLM
STAT- MEDLINE
DCOM- 19940705
LR  - 20131121
IS  - 0021-972X (Print)
IS  - 0021-972X (Linking)
VI  - 78
IP  - 6
DP  - 1994 Jun
TI  - Type 2 11 beta-hydroxysteroid dehydrogenase in human fetal tissues.
PG  - 1529-32
AB  - 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyzes the conversion of 
      active cortisol to inactive cortisone, and regulates the access of cortisol to 
      both the mineralocorticoid and glucocorticoid receptors. Two isoforms of 11 
      beta-HSD have been described, the cloned "type 1" NADP(H)-dependent 
      dehydrogenase/oxo-reductase and a high affinity NAD-dependent dehydrogenase (type 
      2). In the fetus, 11 beta-HSD activity may serve to protect developing tissues 
      from cortisol excess or may modulate the permissive actions of glucocorticoids. 
      We have studied 11 beta-HSD activity and mRNA levels in human mid-gestational 
      fetal tissues. Tissue homogenates were incubated with either 0.1 mumol/L cortisol 
      and 400 mumol/L NAD, 2.5 mumol/L cortisol and 400 mumol/L NADP, or 0.1 mumol/L 
      cortisone wither either 400 mumol/L NADPH or NADH. No activity (< 2.5% 
      conversion) was observed in fetal tissues using either cortisone or 2.5 mumol/L 
      cortisol as a substrate. 11-oxo-reductase activity was observed in 
      maternally-derived decidua. In keeping with these activity studies, northern blot 
      analysis of fetal tissue RNA and PCR-reverse transcriptase of type 1 11 beta-HSD 
      mRNA indicated 11 beta-HSD mRNA in decidua, but failed to detect any type 1 11 
      beta-HSD mRNA transcripts in fetal tissues. In contrast when 0.1 mumol/L cortisol 
      was used as a substrate in the presence of NAD, 11 beta-HSD activity was 
      ubiquitous with highest levels seen in the kidney (131 +/- 16 (SE) pmoles 
      cortisone formed/h/mg.protein) > lung > gonad > liver > colon. 11 beta-HSD 
      activity in fetal tissues is mediated by the type 2, high affinity, isoform. The 
      widespread distribution of this novel isoform suggests that it may play an 
      important role in fetal development. Type 1 11 beta-HSD mRNA and activity are 
      absent in mid-gestational fetal tissues, but present in maternally-derived 
      decidua, suggesting that its ontogeny is a late-gestational of post-natal event.
FAU - Stewart, P M
AU  - Stewart PM
AD  - Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of 
      Texas Southwestern Medical Center, Dallas.
FAU - Murry, B A
AU  - Murry BA
FAU - Mason, J I
AU  - Mason JI
LA  - eng
GR  - HD-11149/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Isoenzymes)
RN  - 0 (RNA, Messenger)
RN  - EC 1.1.- (Hydroxysteroid Dehydrogenases)
RN  - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - 11-beta-Hydroxysteroid Dehydrogenases
MH  - Abortion, Induced
MH  - Decidua/*enzymology
MH  - Female
MH  - Fetus/*enzymology
MH  - *Gene Expression
MH  - Humans
MH  - Hydrocortisone/metabolism
MH  - Hydroxysteroid Dehydrogenases/analysis/*biosynthesis/metabolism
MH  - Isoenzymes/analysis/*biosynthesis/metabolism
MH  - Kinetics
MH  - Male
MH  - Organ Specificity
MH  - Polymerase Chain Reaction
MH  - Pregnancy
MH  - RNA, Messenger/analysis/biosynthesis
MH  - Transcription, Genetic
EDAT- 1994/06/01 00:00
MHDA- 1994/06/01 00:01
CRDT- 1994/06/01 00:00
PHST- 1994/06/01 00:00 [pubmed]
PHST- 1994/06/01 00:01 [medline]
PHST- 1994/06/01 00:00 [entrez]
AID - 10.1210/jcem.78.6.8200959 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 1994 Jun;78(6):1529-32. doi: 10.1210/jcem.78.6.8200959.