The Human Placental Lactogen Genes: Structure, Function, Evolution and Transcriptional Regulation

Walker, William H.; Fitzpatrick, Susan L.; Barrera-Saldaña, Hugo A.; Reséndez‐Pérez, Diana; Saunders, Grady F.

doi:10.1210/edrv-12-4-316

Cited by 136 publications

(89 citation statements)

References 75 publications

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“…At term their levels exceed 0.0 15 ,ug mL . As expected, concentrations of PL and PGH in foetal serum are much lower than concentrations in maternal serum (Frankenne et a!., 1988;Eriksson et al, 1989;Walker et al, 1991). Haig(1993) details further evidence consistent with the involvement of placental lactogens in maternal/f oetal conflict.…”

Section: Ube1x Escapes Inactivation On the Human X Butsupporting

confidence: 75%

Embryonic growth and the evolution of the mammalian Y chromosome. II. Suppression of selfish Y-linked growth factors may explain escape from X-inactivation and rapid evolution of Sry

Hurst¹

1994

Heredity

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The mammalian Y chromosome may be an attractor for selfish growth factors. A suppressor of the selfish growth effects would be expected to spread were it to have an appropriate parent-specific expression rule. A suppressor could act by boosting the resource demands of competing female embryos. This possibility may explain incidences of the escape from X-inactivation and provides a rationale for why these genes typically have Y-linked homologues. Alternatively, a suppressor could act to decrease the resource demands of males with the selfish Y. This possibility is supported by the finding that the size of male, but not female, human infants is negatively correlated to the number of X chromosomes. A protracted arms race between a selfish gene and its suppressor may ensue. Both the variation in copy number of Zfyand the unusually fast sequence evolution of Siy may be explained by such an arms race. As required by the model, human S#y is known to have an X-linked suppressor. Preliminary evidence suggests that, as predicted, rapid sequence evolution of Sry may be correlated with female promiscuity. The case for fast sequence evolution as the product of maternal/foetal conflict is strengthened by consideration of the rapid evolution of placental lactogens in both ruminants and rodents.

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Section: Ube1x Escapes Inactivation On the Human X Butsupporting

confidence: 75%

Embryonic growth and the evolution of the mammalian Y chromosome. II. Suppression of selfish Y-linked growth factors may explain escape from X-inactivation and rapid evolution of Sry

Hurst¹

1994

Heredity

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“…Circulating concentrations of hCS in humans are primarily dependent upon syncytial cell mass, since hCS mRNA concentrations in individual syncytiotrophoblasts do not change throughout pregnancy (Walker et al 1991). Conversely, hCS synthesis per syncytiotrophoblast increases in late pregnancy in the baboon, concomitant with additional syncytiotrophoblast differentiation (Musicki et al 1997).…”

Section: Chorionic Somatomammotropinmentioning

confidence: 99%

GH as a co-gonadotropin: the relevance of correlative changes in GH secretion and reproductive state

Hull

Harvey

2002

Journal of Endocrinology

104

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It is now well established that exogenous GH promotes sexual maturation and reproductive function. The possibility that this may reflect physiological actions of endogenous GH has, however, rarely been considered. Correlative changes in GH secretion and reproductive state (puberty, pregnancy, lactation, menopause and ovarian cycles) are thus the primary focus of this review. GH secretion is, for instance, elevated during major transitions in reproductive status such as puberty and pregnancy. In some cases, augmented circulating GH levels are paired with hepatic GH resistance. This interaction may permit selective activation of gonadal responses to GH without activating IGF-I-mediated systemic responses. This selective activation may also be mediated by autocrine, paracrine or intracrine GH actions, since GH is also synthesized in reproductive tissues. Correlative changes in GH secretion and reproductive state may be mediated by events at the hypothalamic, pituitary and gonadal level. In addition to direct effects on gonadal function, GH may influence reproductive activity by increasing gonadotropin secretion at the hypothalamic and pituitary level and by enhancing gonadotropin responsiveness at the gonadal level. The close association between reproductive status and the somatotrophic axis supports the physiological importance of GH in reproductive function.

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“…The luteal hormone, relaxin, which is increased during pregnancy, also induces vasodilation, although this effect is mediated via increased NO production through the phosphorylation of www.chinaphar.com Gonzalez C et al Acta Pharmacologica Sinica npg endothelial NO synthase (eNOS) [7] . Among the reproductive hormones, the prolactin (PRL) family also exerts controversial vascular effects; the members of the PRL family include growth hormone (GH), placental lactogen (PL) and PRL, hormones that share structural and biological similarities [8][9][10][11][12][13] . GH and PRL are produced primarily in the pituitary gland but may also be locally produced by endothelial cells [1,9,14] .…”

Section: Introductionmentioning

confidence: 99%

The prolactin family hormones regulate vascular tone through NO and prostacyclin production in isolated rat aortic rings

et al. 2015

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Aim: Prolactin family hormones include growth hormone, placental lactogen and prolactin, which are able to regulate angiogenesis via NO and prostaglandins. However, their effects on vascular tone are not fully understood. The aim of this study was to evaluate the effects of prolactin family hormones on rat vascular tone in vitro. Methods: Aortic rings were prepared from adult male rats and precontracted with phenylephrine, then treated with the hormones and drugs. The tension was measured with isometric force displacement transducer connected to a polygraph. NO production and prostacyclin release in physiological solution was determined. Cultured rat aortic endothelial cells (RAECs) were treated with the hormones and drugs, and the phosphorylation of eNOS at serine 1177 was assessed using Western bolt analysis. Results: Administration of growth hormone or placental lactogen (0.01-100 nmol/L) induced endothelium-dependent vasodilation. Both the hormones significantly increased the phosphorylation of eNOS in RAECs and NO level in physiological solution. Preincubation with L-NAME blocked growth hormone-or placental lactogen-induced vasodilation and NO production. Preincubation with an antibody against growth hormone receptors blocked growth hormone-and placental lactogen-induced vasodilation. Addition of a single dose of prolactin (0.01 nmol/L) induced sustained vessel relaxation, whereas multiple doses of prolactin induced a biphasic contractionrelaxation effect. The vascular effects of prolactin depended on endothelium. Prolactin significantly increased the level of prostacyclin I 2 in physiological solution. Preincubation with indomethacin or an antibody against prolactin receptors blocked prolactin-induced vasodilation. Conclusion: The prolactin family hormones regulate rat vascular tone, selectively promoting either relaxation or contraction of vascular smooth muscle via activation of either growth hormone receptors or prolactin receptors within the endothelium.

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The Human Placental Lactogen Genes: Structure, Function, Evolution and Transcriptional Regulation

Cited by 136 publications

References 75 publications

Embryonic growth and the evolution of the mammalian Y chromosome. II. Suppression of selfish Y-linked growth factors may explain escape from X-inactivation and rapid evolution of Sry

Embryonic growth and the evolution of the mammalian Y chromosome. II. Suppression of selfish Y-linked growth factors may explain escape from X-inactivation and rapid evolution of Sry

GH as a co-gonadotropin: the relevance of correlative changes in GH secretion and reproductive state

The prolactin family hormones regulate vascular tone through NO and prostacyclin production in isolated rat aortic rings

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