Synergistic Effect of Triiodothyronine and Dexamethasone on Male and Female Fetal Rat Lung Surfactant Synthesis

Js, Torday; Dow, K

doi:10.1159/000457153

Cited by 36 publications

(18 citation statements)

References 11 publications

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“…Thyroidectomy of fetal sheep reduces the number of type II pneumocytes in the lungs at term as well as the number of surfactantcontaining lamellar bodies in these cells (Ayromlooi et al 1983). In vitro and in vivo studies have shown that thyroid hormones affect synthesis of both the phospholipid and protein components of surfactant in fetal mice, rats, sheep, monkeys, and human infants (Ballard et al 1984, Das et al 1984, Torday & Dow 1984, Warburton et al 1988, Romaguera et al 1993, Gilbert et al 2001, van Tuyl et al 2004. In particular, thyroid hormones promote synthesis of surfactant proteins B and C. They also increase the phospholipid content of lung liquid, although this effect may be mediated via upregulation of pulmonary b-adrenergic receptor expression and, hence, enhanced epinephrine-stimulated surfactant release (Das et al 1984, Warburton et al 1988.…”

Section: The Lungs and Respiratory Functionmentioning

confidence: 99%

Thyroid hormones in fetal growth and prepartum maturation

Forhead

Fowden

2014

Journal of Endocrinology

359

270

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The thyroid hormones, thyroxine (T 4 ) and triiodothyronine (T 3 ), are essential for normal growth and development of the fetus. Their bioavailability in utero depends on development of the fetal hypothalamic-pituitary-thyroid gland axis and the abundance of thyroid hormone transporters and deiodinases that influence tissue levels of bioactive hormone. Fetal T 4 and T 3 concentrations are also affected by gestational age, nutritional and endocrine conditions in utero, and placental permeability to maternal thyroid hormones, which varies among species with placental morphology. Thyroid hormones are required for the general accretion of fetal mass and to trigger discrete developmental events in the fetal brain and somatic tissues from early in gestation. They also promote terminal differentiation of fetal tissues closer to term and are important in mediating the prepartum maturational effects of the glucocorticoids that ensure neonatal viability. Thyroid hormones act directly through anabolic effects on fetal metabolism and the stimulation of fetal oxygen consumption. They also act indirectly by controlling the bioavailability and effectiveness of other hormones and growth factors that influence fetal development such as the catecholamines and insulin-like growth factors (IGFs). By regulating tissue accretion and differentiation near term, fetal thyroid hormones ensure activation of physiological processes essential for survival at birth such as pulmonary gas exchange, thermogenesis, hepatic glucogenesis, and cardiac adaptations. This review examines the developmental control of fetal T 4 and T 3 bioavailability and discusses the role of these hormones in fetal growth and development with particular emphasis on maturation of somatic tissues critical for survival immediately at birth.

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Section: The Lungs and Respiratory Functionmentioning

confidence: 99%

Thyroid hormones in fetal growth and prepartum maturation

Forhead

Fowden

2014

Journal of Endocrinology

359

270

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“…Male fetuses present a transient delay in lung maturation compared with female fetuses (Nielsen & Torday 1981, Torday & Dow 1984, Nielsen 1985 in such a way that preterm delivery leads to a higher incidence of respiratory distress syndrome (RDS or hyaline membrane disease) in males (Farrell & Avery 1975, Papageorgiou et al 1981, Nielsen et al 1982, Perelman et al 1986a. Surfactant deficiency is one major cause of RDS and the surge of surfactant synthesis is normally delayed in the developing male lung when compared with the female (Nielsen & Torday 1981, Torday & Dow 1984, Nielsen 1985.…”

Section: Introductionmentioning

confidence: 99%

“…Surfactant deficiency is one major cause of RDS and the surge of surfactant synthesis is normally delayed in the developing male lung when compared with the female (Nielsen & Torday 1981, Torday & Dow 1984, Nielsen 1985. In fact, the sex difference in surfactant production pertains to its lipid moiety (Nielsen et al 1982, Nielsen 1985, Ballard 1989.…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Provost¹,

Boucher²,

Tremblay³

2008

Journal of Endocrinology

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A sex difference in surfactant lipids is associated with a higher incidence of respiratory distress syndrome for males in cases of preterm birth. In animal models, the sex difference in surfactant lipids was shown to be androgen receptordependent. This report examines expression of apolipoprotein (apo)A-I, apoA-II, apoC-II, apoE, apoH, and lipoprotein lipase (LPL) by quantitative real-time PCR in pools of male and female fetal lung tissues from various mouse litters from gestation day (GD) 15 . 5 to 18 . 5, and in various adult tissues.Although the expression profiles of ApoA-I, ApoA-II, ApoC-II, and ApoH are complex, these genes are co-regulated and they all present a sex difference (PZ0 . 0896, 0 . 0896, 0 . 0195, and 0 . 0607 respectively) with higher expression for females for several litters. Pulmonary expression of apoA-I, apoA-II, and apoH were specific to the developing lung. ApoE and LPL mRNAs showed a significant increase from GD 17 . 5 to 18 . 5. An increase in apoA-I-, apoA-II-, apoC-II-, and apoHmRNA accumulation was observed from GD 16 . 5 to 17 . 5 in correlation with the emergence of mature type II pneumonocytes. These four apolipoprotein genes are co-regulated with type 2 and 5 17b-hydroxysteroid dehydrogenases, which are respectively involved in inactivation and synthesis of androgens. Finally, apoC-II was detected by immunohistochemistry in epithelial cells of the distal epithelium. Positive signals looking like secretory granules were located near the basal membrane. Our results are compatible with a role for apolipoproteins in lipid metabolism and transport in the developing lung in association with the sex difference in surfactant lipid synthesis.

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“…A sexual dimorphism in fetal pulmonary surfactant production has been described (1)(2)(3); it is characterized in many mammalian species by an increase in female fetal surfactant phosThis work was presented in part as an abstract at the annual meeting of the Society for Pediatric Research, May 1983. Received for publication 21 September 1984 and in revised form 5 March 1985. pholipid production. This has been implicated in the clinical observations of greater incidence of the respiratory distress syndrome (RDS)' in male newborns and the failure of male fetuses to respond to prenatal glucocorticoid therapy to protect against RDS (1,4).…”

Section: Introductionmentioning

confidence: 99%

Androgen receptors influence the production of pulmonary surfactant in the testicular feminization mouse fetus.

Nielsen¹

1985

J. Clin. Invest.

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A sexual dimorphism in fetal pulmonary maturation has been described in which the female fetal lung produces surfactant earlier in gestation than the male fetal lung. This is felt to be related to the increased incidence in male newborns of the Respiratory Distress Syndrome. Dihydrotestosterone will delay surfactant production in the female fetus, and a relationship between fetal sexual differentiation and fetal lung maturation has been proposed. We hypothesized that the dimorphism in fetal surfactant production is dependent on androgen receptor function. We measured phosphatidylcholine (PC), saturated phosphatidylcholine (SPC), and sphingomyelin (S) in the amniotic fluid of fetal mice of the mouse model of testicular feminization (Tfm mouse). In this model, male carriers of the X-linked Tfm gene have no functional androgen receptors. The mean amniotic fluid phosphatidylcholine to sphingomyelin ratio (PC/S ratio) was 28% higher in females than in normal males, and the amniotic fluid PC/S ratio of the Tfm male fetuses was the same as the females. The ratio of amniotic fluid saturated phosphatidylcholine to sphingomyelin (SPC/S ratio) was lowest in males, intermediate in females, and highest in Tfm males. A significant relationship between the fetal groups and the amniotic fluid SPC/S ratio was identified by analysis of variance. There were no differences in the whole lung phospholipid content between the three groups.To substantiate the effect of androgen receptors, dihydrotestosterone was injected into pregnant carriers of the Tfm mutation, 2.5 mg/d from day 10 of gestation through the day of sacrifice. The amniotic fluid PC/S ratio was decreased in the female fetuses (consisting of both homozygous normal and heterozygous carriers of the Tfm gene), but not in the Tfm male fetuses. The overall result was no significant difference between the male and female amniotic fluid PC/S ratio while the Tfm amniotic fluid PC/S ratio remained at the level of the untreated females.We conclude that androgens affect fetal lung development via a mechanism dependent on the presence of androgen receptors.

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Synergistic Effect of Triiodothyronine and Dexamethasone on Male and Female Fetal Rat Lung Surfactant Synthesis

Cited by 36 publications

References 11 publications

Thyroid hormones in fetal growth and prepartum maturation

Thyroid hormones in fetal growth and prepartum maturation

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Androgen receptors influence the production of pulmonary surfactant in the testicular feminization mouse fetus.

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