Plasma Corticosterone Levels During Pregnancy in the Mouse: The Relative Contributions of the Adrenal Glands and Foeto-Placental Units

Barlow, Susan; Morrison, P. J.; Sullivan, Frank

doi:10.1677/joe.0.0600473

Cited by 109 publications

(44 citation statements)

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“…In dexamethasone-induced cells and in neonatal liver, the abundance of Amy-J-L transcripts increased approximately 15-fold. Concomitant with the increase in liver amylase just before birth, there is an increase in circulating glucocorticoid levels (2,9,41). This suggests that the Amy-i liver promoter is regulated by glucocorticoids during development in vivo.…”

Section: Resultsmentioning

confidence: 99%

Glucocorticoid and developmental regulation of amylase mRNAs in mouse liver cells.

et al. 1988

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We characterized alpha-amylase expression in the hepatoma cell line Hepa 1-6 and in normal mouse liver. Both Amy-1 and Amy-2 were expressed in Hepa 1-6 and were regulated by glucocorticoids. Transcription in the hepatoma cells was initiated at the same start sites as in mouse tissues. Glucocorticoid treatment increased the abundance of Amy-1 and Amy-2 transcripts by 10 to 20-fold. This increase was detected within 4 h and was maximal by 24 h. The pattern of amylase expression in this hepatoma cell line accurately reflects amylase expression in the liver in vivo. During liver development, we observed a large increase in the abundance of Amy-1 transcripts just before birth, at a time when circulating glucocorticoids are also elevated. Adult mouse liver expressed Amy-1 and Amy-2 at levels comparable to those of fully induced hepatoma cells. Liver is thus a likely source of both amylase isozymes in mouse serum. These studies demonstrate that Amy-2 expression is not limited to the pancreas but also occurs at a low level in liver cells.

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Section: Resultsmentioning

confidence: 99%

Glucocorticoid and developmental regulation of amylase mRNAs in mouse liver cells.

et al. 1988

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“…For the first time, we have shown that throughout pregnancy, the circadian profiles of 11-DHC generally paralleled the corresponding corticosterone profiles, including the apparent loss of rhythmicity on day 18. The ratio of corticosterone:11-DHC increased substantially on day 14, possibly due to greater plasma CBG binding of corticosterone and an associated reduction in the proportion metabolized to 11-DHC (Barlow et al 1974(Barlow et al , 1975. This conversion is catalyzed by the 11b-hydroxysteroid dehydrogenase enzymes (11b-HSD1 and 11b-HSD2), and opposite changes in their expression occur in the two placental zones late in rodent pregnancy (Mark et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Pregnancy-induced adaptations of the central circadian clock and maternal glucocorticoids

Wharfe¹,

Mark²,

Wyrwoll³

et al. 2015

Journal of Endocrinology

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Maternal physiological adaptations, such as changes to the hypothalamic-pituitary-adrenal (HPA) axis, are central to pregnancy success. Circadian variation of the HPA axis is dependent on clock gene rhythms in the hypothalamus, but it is not known whether pregnancy-induced changes in maternal glucocorticoid levels are mediated via this central clock. We hypothesized that hypothalamic expression of clock genes changes across mouse pregnancy and this is linked to altered HPA activity. The anterior hypothalamus and maternal plasma were collected from C57Bl/6J mice prior to pregnancy and on days 6, 10, 14 and 18 of gestation (termZd19), across a 24-h period (0800, 1200, 1600, 2000, 0000, 0400 h). Hypothalamic expression of clock genes and Crh was determined by qPCR, plasma ACTH concentration measured by Milliplex assay and plasma corticosterone concentration by LC-MS/MS. Expression of all clock genes varied markedly across gestation, most notably at mid-gestation when levels of each gene were elevated. The pregnancy-induced increase in maternal corticosterone levels (by up to 14-fold on day 14) was not accompanied by a parallel shift in plasma ACTH (28% lower on day 14 compared with non-pregnant levels). Moreover, while circadian rhythmicity in corticosterone was maintained up to day 14 of gestation, this was effectively lost by day 18. Overall, our data show that the central circadian clock undergoes marked adaptations throughout mouse pregnancy, changes that are likely to contribute to maternal physiological adaptations. Importantly, however, neither hypothalamic clock genes nor plasma ACTH levels appear to drive the marked increase in maternal corticosterone after mid-gestation.

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“…Progesterone may exert its effect on the functional differentiation of T cells partly through GR. During the second half of pregnancy in mice, plasma corticosterone levels reach a peak of 4 M on day 16, ϳ60 times the nonpregnant resting level (45). Most of the plasma corticosterone is of adrenal origin, and the remaining portion of the corticosterone is feto-placental in origin (45).…”

Section: Discussionmentioning

confidence: 99%

Direct and Indirect Inhibition of Th1 Development by Progesterone and Glucocorticoids

Miyaura

Iwata

2002

The Journal of Immunology

323

229

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Progesterone may contribute to the maternal suppression of immunity to the fetus by modulating the Th1/Th2 balance. To clarify whether progesterone directly or indirectly affects T cell differentiation, we used two experimental systems with isolated T cells in vitro. In one system, isolated CD4+CD8+ thymocytes differentiated into Th1 and Th2 by two pulse stimulations with defined combinations of ionomycin and PMA followed by the treatment with IL-12, IL-4, and IL-2. In the second system, functional differentiation was induced in purified naive CD4 T cells with cytokines and Abs to CD3 and CD28. In both systems, progesterone added with cytokines suppressed Th1 development at concentrations associated with pregnancy, but enhanced the development of IL-10-producing Th2 cells. Because IL-10 is known to inhibit APC production of IL-12, Th1 development may be also suppressed indirectly by progesterone. However, progesterone failed to enhance IL-10 production in the absence of IL-12. The p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 inhibited Th1 development and enhanced Th2 development, as did progesterone, indicating that p38 MAPK and extracellular signal-regulated kinase pathways are involved in Th1 development. However, the progesterone effects may not be simply due to a modulation of MAPK activities, because the inhibitor did not significantly affect the development of IL-10-producing cells in the presence or absence of progesterone. Glucocorticoids exerted effects similar to those of progesterone on Th1/Th2 development even at lower concentrations. These results suggest that progesterone as well as glucocorticoids directly inhibit Th1 development and enhance Th2 development.

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Plasma Corticosterone Levels During Pregnancy in the Mouse: The Relative Contributions of the Adrenal Glands and Foeto-Placental Units

Cited by 109 publications

References 0 publications

Glucocorticoid and developmental regulation of amylase mRNAs in mouse liver cells.

Glucocorticoid and developmental regulation of amylase mRNAs in mouse liver cells.

Pregnancy-induced adaptations of the central circadian clock and maternal glucocorticoids

Direct and Indirect Inhibition of Th1 Development by Progesterone and Glucocorticoids

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