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PubMed1982

Glucocorticoid metabolism in human placenta, decidua, myometrium and fetal membranes.

The metabolism of cortisone (E) and cortisol (F) by human placenta, decidua, myometrium, chorion and amnion during pregnancy was studied in vitro. Early pregnancy, midpregnancy and term placentae metabolized F efficiently yielding E as the major product. The capacity of the placenta to inactivate F to E was observed as early as the 8th week of pregnancy and there was a significantly higher (P less than 0.001) net production of E in early pregnancy placenta than in term placenta. In contrast to the placenta, midpregnancy and term decidua metabolized mainly E to F with a net production of F. Term chorion demonstrated an equal degree of oxidative and reductive glucocorticoid metabolism while term amnion and myometrium had negligible metabolic activity. Thus the net production of F from E by the decidual membrane unit is due to metabolic activity in the decidua as early as the 13th week of pregnancy and not to activity in the fetal membranes.

Cortisone↗
PubMed1983

Inhibition of progesterone synthesis in placenta by administration of dexamethasone to pregnant rats.

Glucocorticoid receptors have been detected in placenta from several species, including the rat, although the biological function of corticoids is unknown in placenta from the latter species. The present experiments examined the effect of glucocorticoid treatment on placental progesterone biosynthesis from endogenous precursors by incubated basal zone trophoblast and labyrinthine zone of placentas from adrenalectomized-ovariectomized rats at the end of pregnancy. It was found that a higher proportion of synthesized progesterone was retained in the tissue than that released into the incubation medium. Treatment of rats on the 17th-18th day of pregnancy with 10 micrograms/ml of dexamethasone in the drinking saline for 3 days, produced a significant inhibition of progesterone detected in tissue and medium of incubated placental zones. In vitro addition of dexamethasone (10(-4) M) was also effective in reducing progesterone in the placental zone studied (LZ). Serum progesterone of intact rats was in the range of rats near parturition (approx 25 ng/ml) and dropped to almost undetectable levels in rats with adrenalectomy and ovariectomy, with or without dexamethasone treatment, suggesting that in late pregnancy the rat placenta does not contribute significantly to circulating levels of progesterone. This glucocorticoid effect could not be extended to estrogens, as we, in accord with the work of other groups, failed to detect estrogen synthesis in rat placenta. It is suggested that a function for glucocorticoid receptors in rat placenta may be the inhibition of local progesterone production.

Adrenalectomy↗
PubMed1983

Aromatase activity of steroid sulphatase-deficient placentae.

Aromatase activity was measured in homogenates from steroid sulphatase deficient and steroid sulphatase positive placentae. The activity of the aromatase complex was determined from the rate of formation of [14C] oestrone plus [14C] oestradiol when [14C] testosterone was incubated with a rate-limiting quantity of homogenate. A reduced level of aromatase activity was found in vitro in 70% of steroid sulphatase-deficient placentae tested, but the deficiency was much less complete than that of steroid sulphatase. The mean (+/- SD) aromatase activity of steroid sulphatase-deficient placentae was 380 +/- 180 pmol product/h/g tissue (n = 10), significantly lower (P less than 0.001, t-test) than the mean aromatase activity of steroid sulphatase positive placentae (701 +/- 70 pmol product/h/g tissue, n = 10). Seventy per cent of the steroid sulphatase deficient placentae showed lower aromatase activity than that of normal placentae stored for a comparable period of time. Assay imprecision and the sex of the foetus were excluded as reasons for the diminished aromatase activity found. It may arise through an abnormal gene product and consequent alterations in the structure of the microsomal membrane in which both aromatase complex and steroid sulphatase enzymes are retained.

Acetylation↗
PubMed1991

Histopathological findings in placentae from patients with intra-uterine fetal death and anti-phospholipid antibodies.

Anti-phospholipid antibodies are associated with first trimester abortions and late intra-uterine fetal death. The histopathology of 47 placentae from 45 women with intra-uterine fetal death, including 16 patients with anti-phospholipid antibodies, was studied in order to detect potential differences between placentae from women with and without these antibodies. Thirteen patients had systemic lupus erythematosus or lupus-like disease, including 6 women with anti-phospholipid antibodies. In placentae from patients with anti-phospholipid antibodies, a decrease in vasculo-syncytial membranes, fibrosis mainly in infarcted areas, hypovascular villi and thrombosis or infarction was seen significantly more often than in placentae from women without these antibodies. Of 17 placentae from 16 patients with anti-phospholipid antibodies, only 3 did not demonstrate signs of thrombosis or infarction. Thrombosis/infarction was significantly associated with a decrease in vasculo-syncytial membranes, fibrosis, hypovascular villi and an increase in syncytial knots. These findings are most likely to be the result of prolonged hypoxia due to thrombosis or infarction. It is concluded that thrombosis or infarctions are prominent features in placenta from patients with anti-phospholipid antibodies and intra-uterine fetal death. Consequently, antithrombotic treatment during pregnancy forms a rational approach in these patients.

Adult↗
PubMed1995

Low-dose aspirin: lack of association with an increase in abruptio placentae or perinatal mortality.

OBJECTIVE: To perform a meta-analysis determining the association of low-dose aspirin treatment with subsequent abruptio placentae or perinatal mortality. DATA SOURCES: Studies were identified and selected using the MEDLINE bibliographic data base of entries from January 1985 through April 1994. In addition, a manual search was performed using the references from all retrieved reports, review articles, and chapters from textbooks. METHODS OF STUDY SELECTION: Three criteria were used to select studies for inclusion: 1) Studies were designed as randomized or double-blind clinical trials; 2) aspirin was administered in doses of less than 200 mg/day; and 3) outcome data included the incidence of abruptio placentae and perinatal mortality. Three studies did not report the occurrence of abruptio placentae, but the authors of those papers answered written requests for such data. A total of 11 studies met our inclusion criteria. DATA EXTRACTION AND SYNTHESIS: We independently evaluated the study methods for each trial and abstracted quantitative outcome data. For each outcome, relative risk, risk differences, and 95% confidence intervals were calculated. The diagnosis of abruptio placentae was taken as self-reported in each trial. No trial of low-dose aspirin in pregnancy had predefined criteria for the diagnosis of abruptio placentae, and abruption was not a primary outcome in any of the 11 trials. We combined data from all studies and compared the data from the randomized trials to those from the double-blind studies. CONCLUSION: We found no increased risk for abruptio placentae or increased perinatal mortality in women taking low-dose aspirin.

Abruptio Placentae↗
PubMed1995

Increased risk of placenta previa among women of Asian origin.

OBJECTIVE: To investigate the frequency of placenta previa among Asian women. METHODS: We conducted a population-based case-control study using Washington state birth certificate data from 1984-1987. Our study population included 810 women with pregnancies complicated by placenta previa and 2917 randomly selected controls. Unconditional logistic regression was used to estimate odds ratios (OR) and their 95% confidence intervals (CI), and interaction terms were used to examine effect modification. Potential confounding by maternal age, gravidity and parity, maternal smoking during pregnancy, and a history of abortion or cesarean delivery was adjusted for in the analysis. RESULTS: The frequency of placenta previa during the study period was 3.3 per 1000 live births. Women of Asian origin were 86% more likely (OR 1.86, 95% CI 1.38-2.51) to have a delivery complicated by placenta previa than were white women. This association was stronger among women without a previous live birth (OR 2.51, 95% CI 1.57-4.01) than those who previously had experienced a live birth (OR 1.50, 95% CI 1.01-2.25). CONCLUSION: Asian women residing in the United States are at increased risk of placenta previa. If confirmed by others, our results suggest that obstetricians should consider meticulous ultrasound evaluations during pregnancy to rule out the presence of placenta previa in Asian-American women.

Abortion, Induced↗
PubMed1997

Comparative localization of endothelial and inducible nitric oxide synthase isoforms in haemochorial and epitheliochorial placentae.

The presence and immunolocalization of type II (inducible or macrophage) and type III (endothelial) nitric oxide synthase (NOS) isoforms were compared in the term placentae of humans, rhesus monkeys, baboons, guinea-pigs, rats and sheep using isoform specific antibodies. In the human placenta, intense immunohistochemical staining for type III NOS was seen in syncytiotrophoblast with weaker staining in vascular endothelial cells. Only vascular endothelial cells showed positive III NOS staining in rhesus monkey, baboon, guinea-pig, rat and sheep placentae. No positive type III NOS immunostaining was seen in trophoblast from any non-human placentae. Western blotting revealed a 135-kDa type III NOS species in placental homogenates, semi-purified by ADP-sepharose affinity chromatography, from all the species tested confirming antibody specificity. Type II NOS immunostaining was localized to certain villous stromal cells which also stained for CD14 (a monocyte/macrophage marker) in the placenta of humans, rhesus monkeys, baboons and sheep. No specific immunohistochemical staining for type II NOS or CD14 was noted in the two rodent species, guinea-pig and rat. On Western blots, a 130-kDa type II NOS species was identified in semi-purified placental homogenates of every species except guinea-pig, although weak bands were seen for rhesus monkey and baboon. The failure of the antibodies to show type II NOS in the rat placenta by immunohistochemistry may be due to a difference in antigen conformation from Western blots. As only human placental syncytiotrophoblast expresses type III NOS, the putative functions ascribed to this isoform in syncytiotrophoblast, i.e., to prevent platelet and leucocyte aggregation in the intervillous space and adhesion to the trophoblast surface or to mediate peptide hormone release from trophoblast, may be unique to humans. Alternatively, syncytiotrophoblast-derived NO may fulfill some other unknown function. The similar pattern of expression of type II NOS in those species with villous fetomaternal interdigitation and multivillous fetomaternal blood flow interrelations may represent a more universal role in surveillance and/or protection against maternal insults or pathogens by immunologic activation and subsequent synthesis of nitric oxide which exerts a cytostatic/cytotoxic response.

Animals↗
PubMedDate not supplied

Molecular charge effects on the protein permeability of the guinea-pig placenta.

The effect of molecular charge on protein permeability of the dually perfused guinea-pig placenta has been investigated by measurement of the permeability surface area products (PS) and observation of the ultrastructural localization of cationic horseradish peroxidase (cHRP) and anionic horseradish peroxidase (aHRP) molecules. Steady-state PS calculated from the experimental data was 0.032 +/- 0.0045 and 0.0045 +/- 0.0008 ml min-1 (mean +/- s.e.m.) for cHRP and aHRP respectively (P less than 0.01). The PS for a diffusional marker, 51Cr-ethylenediaminetetraacetic acid, showed no significant difference between the two groups. Ultrastructurally, placentae perfused with cHRP showed fewer microvilli and a dilated interstitial space compared with placentae perfused with aHRP; large vacuoles were also found in the syncytiotrophoblast in the former but not in the latter tissue. Reaction product in placentae perfused with cHRP was localized to the maternal-facing plasma membrane of the syncytiotrophoblast, in vacuoles and vesicles of the syncytiotrophoblast, and also in the basement membrane of the interstitial space, whereas placentae perfused with aHRP only had reaction product in vesicles in the syncytiotrophoblast. These results suggest that anionic sites in the guinea-pig placenta affect its permeability to charged proteins, cationic molecules inducing structural changes associated with increased permeability.

Animals↗
PubMed1995

Nitric oxide synthase activity in placentae from women with pre-eclampsia.

The syncytiotrophoblast (ST) cell layer of the human villous placenta expresses nitric oxide (NO) synthase. Because NO is a potent relaxant of vascular smooth muscle and inhibitor of platelet activity, we postulated that exaggerated intervillous aggregation of platelets and reduced fetoplacental blood flow in pre-eclampsia result from reduced expression of NO synthase (and production of NO) by the ST. Conversion of [3H]arginine to [3H]citrulline and Lineweaver-Burk transformation were used to derive the Vmax and K(M) of NO synthase. Contrary to our expectations, the Vmax was not significantly different between villous placenta obtained from nulliparous normal and pre-eclamptic women (n = 11 each). The Vmax and K(M) were 22.3 +/- 2.3 pmol/mg per min and 1.3 +/- 0.1 microns, and 22.0 +/- 2.7 pmol/mg per min and 1.4 +/- 0.1 microns, for villous placenta from the nulliparous normal and pre-eclamptic women, respectively. The Vmax and K(M) of placental NO synthase were also comparable among multiparous normal and pre-eclamptic women, as well as women with gestational hypertension. When compared with the enzyme activity of the villous, that of the basal plate was reduced by approximately one-half in all placentae. The calcium-independent activity was consistently 40-fold less than the calcium-dependent activity, and it was similar between villous and basal plate, and between placentae from normal and hypertensive women. We suggest that expression of NO synthase is not different in placentae obtained from normal and pre-eclamptic women.

Adult↗
PubMed1995

Selenoprotein P expression in liver, uterus and placenta during late pregnancy.

To identify genes that exhibit increased expression in the placenta during late pregnancy, the technique of differential cDNA library screening was used to isolate a clone subsequently identified as the 3' untranslated region of the mouse selenoprotein p gene. Random primed radiolabelled cDNA probes were constructed from this clone and these probes were used to conduct Northern hybridizations against total RNA purified from mouse placenta, liver (maternal and fetal) and uterus collected sequentially during the latter third of pregnancy. Signal is present in the placenta and beginning 4 days before birth, the level of message increases, reaching maximal levels at term. The level of expression in the placenta at maximum is approximately 25 per cent of that observed in adult liver. In liver obtained from pregnant females, the level of message is increased compared to nonpregnant adults, but returns to normal shortly after birth. Message is also found in the fetal liver beginning at 4 days before birth and exhibits a pattern of expression similar to the placenta. The similarity of expression observed in fetal liver and placenta suggests a coordinated regulation of expression of this gene in these tissues. There is a minimal amount of signal present in the uterus and the expression does not appear to vary. We speculate that selenoprotein p may play a role in the transplacental transport of selenium to the fetus during late pregnancy.

Animals↗
PubMed1984

Phosphorylation of tyrosine in cultured human placenta.

The [32P]phosphoamino acids in proteins of first-trimester and term-cultured human placentas have been separated and their relative amounts have been measured. Significant phosphorylation of tyrosine residues could be detected in the cultured placental tissue at different stages of gestation. The phosphotyrosine accounts for 2-4% of the total acid-stable phosphate in the phosphoamino acids after partial acid hydrolysis. The difference in the extent of [32P]tyrosine in various placentas seems to be a function of biological variation of the individual placentas, rather than a function of placental age and stage of gestation. In contrast, a significant difference in the phosphorylation ratio of serine and threonine could be measured between first-trimester and term placentas. As more evidence is accumulating that protein phosphorylation of tyrosine is involved in the processes of cellular growth and proliferation, our findings of the relatively high tyrosine phosphorylation in human placenta strongly suggest that this type of protein phosphorylation may play an important role in the placental growth and development. Furthermore, these findings may correlate with the existence of the endogenous RNA virus-like particles found in normal human placenta.

Culture Techniques↗
PubMed1988

Regulation of the production of a prolactin-like protein (MRP/PLF) in 3T3 cells and in the mouse placenta.

Mitogen-regulated protein (MRP), a heterogeneously glycosylated mouse protein of Mr 34,000, is in the same protein family as prolactin, growth hormone, and placental lactogen. We show here that the level of translatable MRP mRNA is increased in response to fibroblast growth factor. Also, the amount of MRP secreted by 3T3 cells is modulated by the rate of degradation of newly synthesized MRP in the lysosomes. This is indicated by several results. First, agents that inhibit protein degradation by lysosomal proteases selectively increased by 2- to 6-fold the incorporation of [35S]methionine into MRP. These agents are ammonium chloride, the carboxylic ionophores, monensin and nigericin, and two thiol protease inhibitors, leupeptin and antipain. MRP that has already been secreted is not degraded by 3T3 cells. We examined the developmental appearance of MRP using immunofluorescence microscopy and found MRP localized in the mouse placenta between days 9 and 13 of development. The amount of MRP in the placenta drops suddenly after day 13. Whereas the appearance of MRP in the placenta follows the reported appearance of its mRNA, MRP disappears from the placenta more rapidly than its mRNA. On the basis of the results of our studies with cells in culture we propose that the production of MRP in the placenta is regulated similarly to prolactin. Thus we propose that the initial increase in MRP production in the placenta is due to pretranslational regulation by growth factors, and the later rapid decline is due to posttranslational regulation through degradation in the lysosomes.

Ammonium Chloride↗
PubMed1975

Effect of chorionic gonadotropin, triamcinolone, progesterone and estrogen on enzymes of placenta and liver in rats.

The activity of several enzymes of regulatory importance for the pathways of glycolysis, gluconeogenesis and lipogenesis was investigated in the placenta and liver of pregnant rats and in the liver of non-pregnant female rats. The rats received daily hormonal treatments on Days 15 to 17 of pregnancy and enzyme activities were measured on Day 18. Chorionic gonadotropin induced minor changes in enzyme activity, apart from a decrease in the activity of hepatic enzymes of lipogenesis in non-pregnant rats. Triamcinolone induced a marked increase in enzymes of gluconeogenesis and a decrease in the activity of pyruvate kinase in the liver of pregnant and non-pregnant rats; in contrast, inverse changes in activity, these enzymes were observed in the placenta. This response in the placenta was considered to arise not from direct hormone effect, but from the accompanying hyperglycemia and hyperinsulinemia. Triamcinolone also increased the activity of hepatic acetyl-CoA carboxylase in pregnant and non-pregnant rats, whereas it reduced the activity of this enzyme in the placenta. Estrogen produced changes similar to those of triamcinolone in the liver and placenta, except that it depressed the activity of acetyl-CoA carboxylase in both tissues. Progesterone had little effect on placental and hepatic enzymes. In general, the changes induced by these hormones in the placenta affected fewer enzymes than in the liver, were less extensive in magnitude and not necessarily in the same direction as in the liver. This indicates that the regulatory placental enzymes are subject to specific control mechanisms not necessarily influenced by direct hormone action.

Acetyl-CoA Carboxylase↗
PubMed1983

Phosphorylation of tyrosine in cultured human placenta.

The [32P]phosphoamino acids in proteins of first trimester and term-cultured human placentas have been separated and their relative amounts were measured. A significant phosphorylation of tyrosine residues could be detected in the cultured placental tissue at different stages of gestation. The phosphotyrosine accounts for 2-4% of the total acid-stable phosphate in the phosphoamino acids after partial acid hydrolysis. The difference in the extent of [32P]tyrosine in various placentas seems to be a function of biological variation of the individual placentas, rather than a function of placental age and stage of gestation. In contrast, a significant difference in the phosphorylation ratio of serine and threonine could be measured between first trimester and term placentas. As more evidence is accumulating that protein phosphorylation of tyrosine is involved in the processes of cellular growth and proliferation, our findings of the relatively high tyrosine phosphorylation in human placenta strongly suggest that this type of protein phosphorylation may play an important role in the placental growth and development. Furthermore, these findings may correlate with the existence of the endogenous RNA virus-like particles found in normal human placenta.

Female↗
PubMedDate not supplied

The mid-trimester placenta previa: a prospective follow-up.

One hundred and fifty-six mid-trimester sonograms were performed at our prenatal diagnostic unit. Twenty women were found to have a low-lying placenta or placenta previa and were followed by serial ultrasound examinations to observe changes in placental position. Eighty percent of women, i.e., 16/20, with a low-lying placenta had converted to normal implantation by the time of delivery. Most of the conversions had taken place at approx. 34 weeks of gestation. The patients with mid-trimester low-lying placenta had an increased risk of third-trimester bleeding, abruptio placentae and cesarean sections. The infants were also at risk of premature delivery. Patients with mid-trimester low-lying or placenta previa should be followed by ultrasound to monitor delivery.

Female↗
PubMed1995

Effect of uterine space and fetal sex on conceptus development and in vitro release of progesterone and estrone from regions of the porcine placenta throughout gestation.

Intact (n = 17) and unilaterally hysterectomized-ovariectomized (UHOX, n = 19) gilts were used to study conceptus development and the steroidogenic capability of three regions of the porcine placenta under normal and crowded intrauterine conditions. Gilts were hysterectomized on either Days 30, 50, 70, or 90 of gestation. Placentas were combined according to the sex of the fetus associated with the placental unit, except at Day 30, when all were combined. Placentas were cut into three regions: middle, inner, and polar. Placental tissues were incubated for 0, 1, 5, and 3 hr, and concentrations of progesterone (P4) and estrone (E1) in the incubation medium were determined. Fetal survival rate was greater (P < 0.01, 0.05, and 0.001 at days 50, 70, and 90, respectively) in intact than in UHOX gilts. Placental length and weight, fetal length and weight, and allantoic fluid volume were greater (P < 0.05, 0.001, 0.05, and 0.001, respectively) in intact than in UHOX gilts. P4 concentration was lower (P < 0.001, 0.002, and 0.001 at Days 50, 70, and 90, respectively) in the incubation medium of polar region placenta compared with the other regions. The release of P4 was greater (P < 0.005) from the placentas of intact versus UHOX gilts at Day 90 but was not different at Days 30, 50, or 70. The sex of the fetus did not affect placental P4 release. The region of the placenta affected E1 release at Day 30 (P < 0.01, greater in polar section) and Day 50 (P < 0.06, less in polar section). There was no effect of uterine status on E1 release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Steroid sulfatase in the human ovary and placenta: enzyme kinetics and phosphate inhibition.

In 5 placental homogenates the Km of steroid sulfatase for DHEA sulfate increased from 15.4 in Tris buffer to 26.8 microM in phosphate (both buffers 0.1 M, pH 7.4), P less than 0.05. In 3 pooled ovarian preparations the Km increased from 14.3 microM in Tris to 33.0 microM in phosphate, P less than 0.01. There was no significant difference between the ovarian and placental values for Km in either Tris or phosphate (P greater than 0.5), and the increase in the Km produced by phosphate in ovarian tissue was not significantly different from that in the placenta (P greater than 0.5). In the placentas the Vmax in Tris was 1420 pmol/min/mg protein and this fell to 523 pmol/min/mg protein in phosphate (P less than 0.005). The Vmax was 50-fold higher in the placenta than in the ovary in either Tris or phosphate (both P less than 0.001). In the ovary, the Vmax was 27.6 pmol/min/mg protein in Tris and 11.0 pmol/min/mg protein in phosphate (P less than 0.05). The reduction of Vmax produced by phosphate in the ovary was not significantly different from that in the placenta (P greater than 0.5). The slope of the 1/v vs 1/S plot (Km/Vmax) increased 4.7-fold in the placentas and 5.8-fold in the ovaries in phosphate over that in Tris (both P less than 0.001); the increase in the placentas was not significantly different from that in the ovaries (P greater than 0.5). Phosphate ion acts as a mixed inhibitor of both placental and ovarian steroid sulfatase.

Arylsulfatases↗
PubMed1995

Co-expression of two distinct isoforms of 11 beta-hydroxysteroid dehydrogenase in the ovine placenta.

We have previously described two distinct isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) with respect to enzymatic activity in the ovine liver and kidney. To determine which isoform(s) is expressed in the ovine placenta, we studied the characteristics of 11 beta-HSD activity in placental tissues collected at days 140-143 of pregnancy. 11 beta-HSD activity was determined by a radiometric conversion assay using cortisol and cortisone as physiological substrates. At 100 nM cortisol, the placental 11 beta-HSD utilized NAD as cofactor, but displayed preference for NADP at 10 microM cortisol. Kinetic characteristics were examined in the presence of alternate cofactors, in order to determine whether this difference in the cofactor requirement represents distinct enzymes. With NAD as cofactor, the placental 11 beta-dehydrogenase had a Km (110 +/- 18 nM) compatible with the kidney enzyme, but displayed a Km (12 +/- 2 microM) similar/identical to the liver 11 beta-HSD when NADP was used. By contrast, the placental 11-oxoreductase showed preference for NADPH regardless of cortisone concentration. Kinetic analysis, using NADPH as cofactor, revealed a single species of 11-oxoreductase activity with a Km of 4 +/- 0.9 microM and a Vmax of 3.1 +/- 0.5 pmol/mg/min. Finally, since the NAD-dependent 11 beta-HSD in the ovine placenta displayed similar/identical kinetic characteristics to the enzyme described previously in the ovine kidney where a truncated 11 beta-HSD transcript was identified, we have also determined whether this transcript is expressed in the placenta by Northern blotting. It was found that the truncated 11 beta-HSD transcript was undetectable in the total RNA samples. These results demonstrate that both liver- and kidney-types of 11 beta-HSD activities are expressed in the ovine placenta, thus providing further evidence for the existence of a NAD-dependent 11 beta-HSD distinct from the well-characterized hepatic NADP-dependent enzyme. Furthermore, the lack of the truncated 11 beta-HSD transcript in the placenta suggests that the NAD-dependent enzyme identified in placenta and kidney is the product of a gene distinct from 11 beta-HSD.

11-beta-Hydroxysteroid Dehydrogenases↗