Uteroferrin : a mechanism of maternal to fetal iron transport in swine / by Charles Andrew Ducsay.

Ducsay, Charles A.

doi:10.5962/bhl.title.42593

Cited by 3 publications

(3 citation statements)

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“…We inferred, extrapolating from our in vitro findings, that chronic maternal melatonin suppression would result in unrestrained actions of fetal ACTH and CRH on the fetal adrenal and, in particular, would allow fetal ACTH to induce fetal adrenal 3β-HSD. The capuchin monkey adrenal gland experiences minor changes during the first week of life, as reported in other primates (McNulty et al 1981;Serón-Ferré & Jaffe, 1981;Ducsay et al 1991;Mesiano & Jaffe, 1997). Therefore an increased adrenal capacity to produce cortisol, acquired during fetal life because of chronic melatonin suppression leading to increased 3β-HSD expression, should be maintained in the early newborn.…”

Section: Discussionmentioning

confidence: 78%

“…The capuchin monkey fetal adrenal gland was remarkably similar to the human and other primates in terms of development (Serón-Ferré & Jaffe, 1981;Mesiano & Jaffe, 1997;McNulty et al 1981;Ducsay et al 1991). The capuchin monkey fetal adrenal increased notably in size between 90 and 141 days of gestation (Fig.…”

Section: Histology and Growth Pattern Of The Capuchin Monkey Adrenal mentioning

confidence: 72%

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Maternal melatonin selectively inhibits cortisol production in the primate fetal adrenal gland

Torres-Farfán¹,

Richter²,

Germaín³

et al. 2004

The Journal of Physiology

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We tested the hypothesis that in primates, maternal melatonin restrains fetal and newborn adrenal cortisol production. A functional G-protein-coupled MT1 membrane-bound melatonin receptor was detected in 90% gestation capuchin monkey fetal adrenals by (a) 2-[125 I] iodomelatonin binding (K d , 75.7 ± 6.9 pM; B max , 2.6 ± 0.4 fmol (mg protein) −1 ), (b) cDNA identification, and (c) melatonin inhibition of adrenocorticotrophic hormone (ACTH)-and corticotrophin-releasing hormone (CRH)-stimulated cortisol but not of dehydroepiandrosterone sulphate (DHAS) production in vitro. Melatonin also inhibited ACTHinduced 3β-hydroxysteroid dehydrogenase mRNA expression. To assess the physiological relevance of these findings, we next studied the effect of chronic maternal melatonin suppression (induced by exposure to constant light during the last third of gestation) on maternal plasma oestradiol during gestation and on plasma cortisol concentration in the 4-to 6-day-old newborn. Constant light suppressed maternal melatonin without affecting maternal plasma oestradiol concentration, consistent with no effect on fetal DHAS, the precursor of maternal oestradiol. However, newborns from mothers under constant light condition had twice as much plasma cortisol as newborns from mothers maintained under a normal light-dark schedule. Newborns from mothers exposed to chronic constant light and daily melatonin replacement had normal plasma cortisol concentration. Our results support a role of maternal melatonin in fetal and neonatal primate cortisol regulation.

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Section: Discussionmentioning

confidence: 78%

Section: Histology and Growth Pattern Of The Capuchin Monkey Adrenal mentioning

confidence: 72%

Maternal melatonin selectively inhibits cortisol production in the primate fetal adrenal gland

Torres-Farfán¹,

Richter²,

Germaín³

et al. 2004

The Journal of Physiology

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“…These results do indicate that there is not an obligatory relationship between fetal weight and albumin and suggest that AFP levels may be influenced by the number of embryos present in early development. It is possible that liver growth as well as function was affected independent of fetal weight; however, it is generally agreed that liver weight is highly correlated with fetal weight even though liver weight expressed as a percentage of fetal body weight decreases rapidly early in development (Dusay, 1980;Pomeroy, 1960). It is perhaps relevant that Ezekwe (1981) recently reported that liver weights of newborn pigs were reduced by maternal starvation while birth weights were not affected.…”

Section: +~=8mentioning

confidence: 99%

The Relationship of Fetal Weight to Serum Albumin and Alpha-Fetoprotein in Swine

Stone¹,

Christenson²

1982

Journal of Animal Science

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The within-litter relationship of fetal weight to fetal serum albumin and alpha-fetoprotein (AFP) was investigated at d 30 to 40, 45 to 50, 50 to 60, 75 to 85 and 90 to 105 of gestation in swine. Regression equations were calculated on individual litters and regression coefficients pooled across litters within each gestational age group. Coefficients for the regression of albumin on fetal weight (microgram . ml-1 . g fetus-1) were significant over all groups and ranged from 22.5 +/- 6.6 to d 45 to 50 to .7 +/- .2 at d 95 to 105. There was no significant relationship between AFP levels and fetal weight at any gestational age. Unilateral ovariectomy-hysterectomy was performed before mating to study effects of uterine crowding on the relationship of fetal weight to AFP and albumin. Although the total number of ovulations was not different from controls, this treatment resulted in only about 1.3 more fetuses/uterine horn compared with controls at either d 40 or 60 of gestation. Fetal weights in crowded litters were not different from controls. However, AFP levels in fetuses from crowded litters were lower than in control fetuses at d 40 (4.5 +/- .1 vs 6.7 +/- .5 mg/ml). Albumin levels in crowded fetuses were significantly lower than in controls at d 60 (342 +/- 50 vs 653 +/- 41 micrograms/ml). Because none of these differences in albumin or AFP could be attributed to variation in fetal weight or fetal number at the time of sample collection, it is possible that more extreme uterine crowding earlier in development resulted in these differences. These results demonstrate that fetal serum albumin concentrations are related to fetal weight when analyzed on a within-litter basis and that unilateral ovariectomy-hysterectomy may affect serum concentrations of both AFP and albumin early in fetal development. Future studies involving the regulation of synthesis of these proteins at the cellular level during development should provide information as to how factors affecting overall fetal growth and development influence the expression of a single gene. Previously, such markers that are amenable to study early in development have been lacking.

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Placental Transport and Distribution of Uteroferrin in the Fetal Pig

Renegar

Bazer

Roberts

1982

Biology of Reproduction

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Placental transport of uteroferrin (Uf), the progesterone-induced iron transport glycoprotein, and its distribution within the fetus were investigated by the peroxidase-antiperoxidase bridge (PAP) technique. In Experiment 1, Uf was localized in endometrial and placental tissues taken from gilts on Days 60, 75, 90 and 105 of pregnancy. Uteroferrin was observed within cells of the endometrial glands and surface epithelium adjacent to placental areolae but not in endometrial surface epithelium between areolae. Heavy staining for Uf was observed in cells of the areolae and was associated with both supra- and infranuclear cytoplasmic vesicles. Vesicles located within the infranuclear cytoplasm were occasionally observed to be releasing their contents into capillaries surrounding the areolae. In Experiment 2, Uf was measured by radioimmunoassay in blood samples taken from the umbilical vein and artery of fetuses on Day 75 of pregnancy. Uteroferrin concentrations were greater (P less than 0.07) in umbilical vein blood (79.8 +/- 13.1 ng/ml) than in umbilical artery blood (43.9 +/- 13.1 ng/ml). Uteroferrin binding by Day 75 fetal liver membranes was examined in Experiment 3. Binding of 125I-Uf increased linearly with increasing quantities of membrane protein and binding of 125I-Uf was competitively inhibited by adding unlabeled Uf to the assay. In Experiment 4, urine samples were taken from Day 75 fetuses and assayed for beta-mercaptoethanol activated acid phosphatase activity which is indicative of Uf. In addition, urine proteins were analyzed for Uf by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and Ouchterlony double immunodiffusion (ID). Acid phosphatase specific activity was 3.37 +/- 1.83 mumol substrate hydrolyzed/10 min per mg protein. Uteroferrin was detected in two of three urine samples by 2D-PAGE and in three of eight samples by ID. In Experiment 5, tissue distribution of Uf was determined by the PAP technique in liver and kidney tissue taken from fetuses on Day 75 of pregnancy. Staining for Uf was observed in collecting ducts and proximal tubules of kidney tissue, but staining was not observed in liver tissue. These results indicate that Uf is transported by the areolae into the chorioallantoic capillaries and to the fetus by the umbilical vein. Within the fetus Uf is either bound by the liver, probably to supply iron for hematopoiesis, or cleared by the kidney and transported within the urine to the allantoic sac to serve as a temporary iron storage reservoir.

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Uteroferrin : a mechanism of maternal to fetal iron transport in swine / by Charles Andrew Ducsay.

Cited by 3 publications

References 88 publications

Maternal melatonin selectively inhibits cortisol production in the primate fetal adrenal gland

Maternal melatonin selectively inhibits cortisol production in the primate fetal adrenal gland

The Relationship of Fetal Weight to Serum Albumin and Alpha-Fetoprotein in Swine

Placental Transport and Distribution of Uteroferrin in the Fetal Pig

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