Developmental changes in lysophospholipid receptor expression in rodent heart from near-term fetus to adult

2012 ◽  
Vol 39 (9) ◽  
pp. 9075-9084 ◽  
Author(s):  
Fang Wang ◽  
Jianfeng Hou ◽  
Bianmei Han ◽  
Yu Nie ◽  
Xiangfeng Cong ◽  
...  
1998 ◽  
Vol 10 (5) ◽  
pp. 393 ◽  
Author(s):  
Alison J. Forhead ◽  
Robert Melvin ◽  
Vanessa Balouzet ◽  
Abigail L. Fowden

Relationships between plasma angiotensin-converting enzyme (ACE) and cortisol, and blood pressure were examined in chronically catheterized ewes and their fetuses during late gestation (111–141 days, term 145 2 days). Plasma ACE was also measured in non-pregnant adult ewes and in lambs over the first 5 weeks of life. In fetuses near term (136–141 days), plasma ACE was greater than in those studied earlier in gestation; overall, plasma ACE correlated with gestational age (r = 0.72). The ontogenic rise in plasma ACE was associated with prepartum increases in plasma cortisol (r = 0.67) and blood pressure (r = 0.66). No relationship was observed between plasma ACE and partial pressure of oxygen in utero. Peak plasma ACE concentration observed in fetuses near term was maintained in newborn lambs for 3 days after birth. By 2 weeks of postnatal age, plasma ACE had decreased to the value seen in non-pregnant adult ewes. Maternal plasma ACE was similar at all gestational ages studied, and was lower than that observed in non-pregnant ewes. Therefore, in the sheep fetus, plasma ACE increased towards term in association with the prepartum cortisol surge. Developmental changes in ACE activity may be partly responsible for the ontogenic rise in fetal blood pressure.


1993 ◽  
Vol 5 (5) ◽  
pp. 479 ◽  
Author(s):  
BJ Waddell

The human placenta appears capable of providing trophic support for the maternal and fetal adrenal cortices. This effect could be mediated both directly, through placental secretion of ACTH1-39 and other peptides, and indirectly via placental CRH1-41 stimulation of pituitary ACTH1-39 secretion. Thus, the placenta is likely to influence the progressive changes that occur in the maternal HPA axis during pregnancy and to promote the developmental changes that occur in the fetal HPA axis. These effects are likely to be of particular importance near term, when the maternal and fetal HPA axes are maximally active and the fetus is dependent upon elevated glucocorticoid levels for maturation of organ systems. Finally, evidence from a variety of studies implicates placental CRH1-41 and ACTH1-39 in the cascade of events involving glucocorticoids and prostaglandins that culminates in parturition.


2017 ◽  
Vol 64 (2) ◽  
pp. 300-311 ◽  
Author(s):  
Dmitry A. Sibarov ◽  
Yulia D. Stepanenko ◽  
Ivan V. Silantiev ◽  
Polina A. Abushik ◽  
Tatiana V. Karelina ◽  
...  

2015 ◽  
Vol 117 (6) ◽  
pp. 559-565 ◽  
Author(s):  
Qingyun Guo ◽  
Yulan Dong ◽  
Jing Cao ◽  
Zixu Wang ◽  
Ziqiang Zhang ◽  
...  

Endocrinology ◽  
1999 ◽  
Vol 140 (11) ◽  
pp. 5233-5238 ◽  
Author(s):  
Junko Matsuda ◽  
Ichiro Yokota ◽  
Yoshihiro Tsuruo ◽  
Takashi Murakami ◽  
Kazunori Ishimura ◽  
...  

1996 ◽  
Vol 135 (5) ◽  
pp. 583-590 ◽  
Author(s):  
Yu M Yu ◽  
Horacio M Domené ◽  
Jorge Sztein ◽  
Debra R Counts ◽  
Fernando Cassorla

Yu YM, Domené HM, Sztein J, Counts DR, Cassorla F. Developmental changes and differential regulation by testosterone and estradiol of growth hormone receptor expression in the rabbit. Eur J Endocrinol 1996;135:583–90. ISSN 0804–4643 To investigate the effects of testosterone and estradiol (E2) on growth hormone receptor (GH-R) gene expression, we measured GH-R mRNA levels in relation to the changes of sex steroid concentrations in the normal male rabbits aged 1–12 months and after administration of testosterone or E2 to castrated male rabbits. In the normal animals, E2 levels were below the detection limit in all age groups, and testosterone levels were below the detection limit at 1 month, increased at 2 months and reached the plateau of the adult levels after 4 months. Liver GH-R mRNA levels were low at 1 month, reached a peak at 2 months and then decreased slightly thereafter. In the castrated animals, liver and growth plate GH-R mRNA levels were increased in the testosterone-treated group (162.0 ± 12.0%, p < 0.025; 128.4 ± 7.6%; p < 0.025) and reduced in the E2-treated group (29.6 ± 6.2%, p < 0.005; 53.6 ± 11.3%, p < 0.025). Sex steroid administration did not result in any significant change in GH-R mRNA levels in striated muscle, kidney and heart. Serum GH concentrations were increased in E2 (15.3 ± 7.7 μg/l vs 4.8 ± 2.2 μg/l, p < 0.025) but the increase was not significant in testosterone-treated animals (8.4 ± 7.7 μg/l vs 4.8 ± 2.2 μg/l). Both testosterone and E2 treatment resulted in a reduction of mean serum growth hormone-binding protein (GHBP) levels compared to control animals (1077 ± 422 pmol/l, p < 0.01; 1137 ± 443 pmol/l, p < 0.01; 2308 ± 565 pmol/l). We conclude that in addition to their stimulatory effect on GH secretion, testosterone and E2 have opposite effects on GH-R gene expression in liver and growth plate in the rabbit. The modulation of GH-R expression by sex steroids may be important for growth during sexual maturation in mammals. Yu M Yu, MD, 11600 Bootjack Court, Gaithersburg, MD 20878, USA


1994 ◽  
Vol 143 (3) ◽  
pp. 505-513 ◽  
Author(s):  
P J Burton ◽  
B J Waddell

Abstract The enzyme 11β-hydroxysteroid dehydrogenase (11β-HSD) catalyses the interconversion of corticosterone, the major glucocorticoid of the rat, and the biologically-inactive 11-dehydrocorticosterone. In the placenta, 11β-HSD is thought to regulate glucocorticoid transport between maternal and fetal compartments, and may also affect the local action of glucocorticoids. The present study assessed whether 11β-dehydrogenase (corticosterone to 11-dehydrocorticosterone) and 11-oxoreductase (11-dehydrocorticosterone to corticosterone) activities are both present in rat placenta, and whether these activities change with advancing pregnancy. Enzyme activity was estimated on days 16, 19 and 22 of pregnancy (term=day 23) in placental fragments incubated for 6 h with either [3H]corticosterone or [3H] 11-dehydrocorticosterone. The percentage conversion of these substrates to [3H] 11-dehydrocorticosterone and [3H] corticosterone, respectively, were determined at the end of the incubation. Both 11-oxoreductase and 11β-dehydrogenase activities were clearly evident in placental tissue fragments, and while 11-oxoreductase activity declined with advancing pregnancy (P<0·01), 11β-dehydrogenase activity increased (P<0·01). Thus, 11-oxoreductase exceeded (P<0·05) 11β-dehydrogenase at day 16, but thereafter activities were similar. These changes do not appear to be glucocorticoid-induced, since pretreatment of rats with either metyrapone or dexamethasone acetate from day 15 of pregnancy did not affect placental 11β-HSD on day 22. To allow comparison with earlier studies, estimates of 11β-HSD were also made in placental homogenates at each stage of pregnancy. In contrast to observations in placental fragments, 11β-dehydrogenase was always the dominant reaction in homogenates, presumably due to the loss of 11-oxoreductase activity following tissue homogenisation. These data demonstrate that net 11β-dehydrogenase activity in the rat placenta increases towards term, thereby increasing the capacity for placental inactivation of active glucocorticoid. This pattern of 11β-HSD is consistent with reduced transfer of active glucocorticoid between the mother and fetus near term, and thus should promote independence of their hypothalamic-pituitary-adrenal axes. Journal of Endocrinology (1994) 143, 505–513


1997 ◽  
Vol 771 (1) ◽  
pp. 142-146 ◽  
Author(s):  
Katherine M Flynn ◽  
Martin P Schreibman ◽  
Lucia Magliulo-Cepriano

2007 ◽  
Vol 58 ◽  
pp. S192
Author(s):  
Hisahiko Kubota ◽  
Henrik Alle ◽  
Heinrich Betz ◽  
Jeorg R.P. Geiger

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