Evidence for the Synthesis of Corticosteroid-Binding Globulin in Human Placenta

Misao, Ryou; Iwagaki, Shigenori; Sun, Wen-Shu; Fujimoto, Jiro; Saio, Masanao; Takami, Taro; Tamaya, Teruhiko

doi:10.1159/000023351

Cited by 20 publications

(16 citation statements)

References 35 publications

(35 reference statements)

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“…CBG may be narrowly expressed in human tissues, with definite tissue expression demonstrated in hepatocytes and in placental syncytiotrophoblasts (24) where CBG may modulate glucocorticoid and progesterone tissue interactions (2). CBG has been reported in rodent adipose tissue by corticosterone binding but not gene expression (11,12), and this may represent circulating CBG from plasma taken into cells.…”

Section: Discussionmentioning

confidence: 99%

“…A negative control, with no reverse transcriptase added, was included for each RNA sample. Previously published CBG (24) and GAPDH (8) primer sequences and a second set of CBG primers we designed (sense 5Ј-GACAAGGGGAAGATGAACAC-3Ј, antisense 5Ј-GCACAGCTTTATGGACCAC-3Ј) were obtained commercially. The PCR was performed in a Corbett Research PC-90 microplate thermal sequencer with an annealing temperature of 55°C and 2 mM MgCl2, these parameters having been optimized for the primers by use of HepG2 cDNA as the positive control.…”

Section: Methodsmentioning

confidence: 99%

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Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Joyner

Hutley

Bachmann

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Glucocorticoids are pivotal for adipose tissue development. Rodent studies suggest that corticosteroid-binding globulin (CBG) modulates glucocorticoid action in adipose tissue. In humans, both genetic CBG deficiency and suppressed CBG concentrations in hyperinsulinemic states are associated with obesity. We hypothesized that CBG deficiency in humans modulates the response of human preadipocytes to glucocorticoids, predisposing them to obesity. We compared normal preadipocytes with subcultured preadipocytes from an individual with the first ever described complete deficiency of CBG due to a homozygous null mutation. CBG-negative preadipocytes proliferated more rapidly and showed greater peroxisome proliferator-activated receptor-γ-mediated differentiation than normal preadipocytes. CBG was not expressed in normal human preadipocytes. Glucocorticoid receptor number and binding characteristics and 11β-hydroxysteroid dehydrogenase activity were similar for CBG-negative and normal preadipocytes. We propose that the increased proliferation and enhanced differentiation of CBG-negative preadipocytes may promote adipose tissue deposition and explain the obesity seen in individuals with genetic CBG deficiency. Furthermore, these observations may be relevant to obesity occurring with suppressed CBG concentrations associated with hyperinsulinemia.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Joyner

Hutley

Bachmann

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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“…Female pups have higher circulating concentrations of CBG resulting in decreased corticosterone negative feedback upon immune and HPA function relative to male pups (McCormick et al 2002;Shanks et al 1994). In the human placenta, cortisol bioavailability is probably controlled by 11β-HSD 2 activity (Patel et al 1999) and possibly CBG (Dancis et al 1978;Misao et al 1999;Benassayag et al 2001). However, no sex-specific differences are known in placental CBG.…”

Section: Sex-specific Differences Of Fetal Immunitymentioning

confidence: 99%

Sexually dimorphic effects of maternal asthma during pregnancy on placental glucocorticoid metabolism and fetal growth

Clifton

2005

Cell Tissue Res

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Human pregnancy is associated with sexually dimorphic differences in mortality and morbidity of the fetus with the male fetus experiencing the poorest outcome following complications such as pre-eclampsia, pre-term delivery and infection. The physiological mechanisms that confer these differences have not been well characterised in the human. Work conducted on the effect of maternal asthma during pregnancy, combining data collected from the mother, placenta and fetus has found some significant sex-related mechanistic differences associated with fetal growth in both normal pregnancies and pregnancies complicated by asthma. Specifically, sexually dimorphic differences have been found in placental glucocorticoid metabolism in male and female fetuses of normal pregnancies. In response to the presence of maternal asthma, only the female fetus alters placental glucocorticoid metabolism resulting in decreased growth. The male fetus does not alter placental function or growth in response to maternal asthma. As a result of the alterations in glucocorticoid metabolism in the female, downstream changes occur in pathways regulated by glucocorticoids. These data suggest that the female fetus adjusts placental function and reduces growth to compensate for maternal disease. However, the male fetus continues to grow in response to maternal asthma with no changes in placental function. This response by the male fetus may partially contribute to the increased risk of morbidity and mortality in this sex.

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“…We also measured the binding properties of CBG before and after removal of endogenous ligands to assess the influence of the steroid and lipid environments in each compartment on the CBG be- havior. Finally, we used reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting to test the capacity of trophoblastic cells from human term placenta to produce CBG mRNA and protein [17].…”

Section: Introductionmentioning

confidence: 99%

Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

Benassayag

Souski

Mignot

et al. 2001

Biology of Reproduction

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The status of the corticosteroid-binding globulin (CBG) at the fetomaternal interface, especially in the maternal intervillous blood space (I), was investigated and compared to that of CBG in the maternal (M) and fetal (umbilical arteries [A] and vein [V]) peripheral circulations at term. Immunoquantitation of plasma CBG showed that the CBG concentration in I was 30% less than that in M (P < 0.001) and threefold higher than that in umbilical cord blood (P < 0.001). The microheterogeneity of CBG studied by immunoaffinoelectrophoresis in the presence of concanavalin A and Western blotting indicated that the CBG in I was mainly of maternal origin and different from fetal CBG. A CBG mRNA, but no classic 50- to 59-kDa CBG, was found in isolated term trophoblastic cells. The steroid environment of the CBG in I differed greatly from that in the peripheral maternal and fetal circulations, because the progesterone:cortisol molar ratio in I was 75-fold higher than that in M and 7- to 10-fold higher than that in the fetal circulation. Binding studies revealed that the affinity constants of CBG for cortisol in I, A, and V were significantly lower than that in M plasma (P < 0.02) in their respective hormonal contexts. The binding parameters for I-CBG stripped of endogenous steroids and lipids were close to those for M-CBG but different from those of fetal CBG (P < 0.001). These data reflect the physiological relevance of the CBG-steroid interaction, especially with very CBG-loaded progesterone at the fetomaternal interface during late pregnancy.

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Evidence for the Synthesis of Corticosteroid-Binding Globulin in Human Placenta

Cited by 20 publications

References 35 publications

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Greater replication and differentiation of preadipocytes in inherited corticosteroid-binding globulin deficiency

Sexually dimorphic effects of maternal asthma during pregnancy on placental glucocorticoid metabolism and fetal growth

Corticosteroid-Binding Globulin Status at the Fetomaternal Interface During Human Term Pregnancy1

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