Transplacental Transfer of a Growth Hormone-Releasing Hormone Peptide from Mother to Fetus in the Rat

Fiorotto, Marta L.; Lopez, Rusmely; Oliver, W. T.; Khan, Amir S.; Draghia-Akli, Ruxandra

doi:10.1089/dna.2006.25.429

Cited by 7 publications

(6 citation statements)

References 43 publications

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“…For instance, gilts treated in the last part of gestation with a HV-GHRHexpressing plasmid had heavier piglets, and the offspring's postnatal growth rate and welfare was enhanced. Changes in pituitary cell lineage in the offspring of treated pregnant sows and rats have been shown, with higher numbers of GH and PRL-producing cells, which can then directly impact their growth and welfare once the postnatal growth comes under the control of GH and IGF-I (Khan et al, 2003;Fiorotto et al, 2006). The increased growth in offspring is not due to maternal pregnancy diabetes (glucose and insulin were normal in all studies, including this one).…”

mentioning

confidence: 60%

Effects of Plasmid Growth Hormone–Releasing Hormone Treatment during Heat Stress

Brown¹,

Bodles-Brakhop²,

Draghia-Akli³

2008

DNA and Cell Biology

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A gene therapy treatment with plasmid-based growth hormone-releasing hormone (GHRH) delivered by electroporation (EP) was investigated during heat stress; 32 primiparous cows received 2.5 mg of a GHRH-expressing myogenic plasmid (pSP-HV-GHRH), while 20 were designated as controls. Offspring of treated animals showed a reduction in mortality (47%; p < 0.02), and survival from birth to 260 days was dramatically improved (0% mortality vs. 21% in controls) along with an increase in weight gain (p < 0.05). Milk production was increased compared to controls with an average yield gain of 421 kg/cow (p = 0.028). Prolactin (PRL) levels were also significantly increased compared to controls (p < 0.05). The second pregnancy rate was improved by GHRH treatment (53.3% vs. 30.8%). This study shows that the use of plasmid-mediated therapy delivered by EP can maintain health status during periods of heat stress, important for both animals and potentially humans in hot, challenging climates.

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mentioning

confidence: 60%

Effects of Plasmid Growth Hormone–Releasing Hormone Treatment during Heat Stress

Brown¹,

Bodles-Brakhop²,

Draghia-Akli³

2008

DNA and Cell Biology

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“…Also importantly, no adverse maternal effects were reported in these studies of GHRH-transduced dams studied throughout the three pregnancies following GHRH plasmid incorporation (Person et al 2008). The variant form of human GHRH, used to electroporate sows in the studies described above, crosses the rat placenta (Fiorotto et al 2006), while circulating GHRH is elevated at birth in progeny of GHRH-plasmid-treated pigs (Khan et al 2003), and circulating IGF1 is elevated in progeny of GHRH-plasmid-treated rats (Khan et al 2002). Effects of elevated maternal GHRH are therefore likely to reflect direct effects on the developing fetus in addition to effects on the maternal GH axis.…”

Section: Strategies To Increase Maternal Ghmentioning

confidence: 91%

The growth hormone–insulin-like growth factor axis in pregnancy

Kaur

Mühlhäusler

Roberts

et al. 2021

Journal of Endocrinology

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The growth hormone (GH)–insulin-like growth factor (IGF) axis is one of the main drivers of mammalian growth and development. Pituitary secretion of GH is pulsatile and under positive and negative hypothalamic control, as well as stimulation from gastric-secreted acyl-ghrelin. GH has anabolic and metabolic effects both directly via the GH-receptor (GHR) and indirectly via stimulation of IGF1 production at multiple target tissues. In this review, we describe the major changes to this axis during pregnancy, with increasing GH abundance in the maternal circulation across multiple species. This stimulates secretion of IGFs, whose bioavailability is also increased by proteolytic cleavage of their circulating binding proteins during pregnancy. These changes in turn induce maternal metabolic adaptations to pregnancy and promote placental function and fetal growth, as does exogenous GH or IGF treatment in animal models of normal and compromised pregnancy. Finally, we explore alternative approaches to enhance maternal GH abundance during pregnancy to promote maternal adaptations, placental function and hence fetal growth.

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“…32 Fioretto et al found a transplacental transfer of a GHRH analog from mother to fetus in the rat. 33 Based on these studies, an effect of GHRH antagonists on a fetus cannot be excluded and therefore pregnancy is contraindicated during therapy with these compounds. However, given the rather short half-life of GHRH antagonists, pregnancy can be planned directly after stopping the treatment.…”

Section: Discussionmentioning

confidence: 99%

Effects of an Antagonistic Analog of Growth Hormone-Releasing Hormone on Endometriosis in a Mouse Model and In Vitro

et al. 2017

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Endometriosis is a benign gynecologic disorder causing dysmenorrhea, pelvic pain, and subfertility. Receptors for the growth hormone-releasing hormone (GHRH) were found in endometriotic tissues. Antagonists of GHRH have been used to inhibit the growth of endometriotic endometrial stromal cells. In this study, the GHRH receptor splice variant (SV) 1 was detected in human endometrial tissue samples by Western blots and quantitative reverse transcription polymerase chain reaction (qRT-PCR). The highest messenger RNA (mRNA) and protein levels of SV1 were found in eutopic endometrium from patients with endometriosis compared to ectopic endometriotic tissues and endometrium from normal patients. The highest expression for GHRH mRNA was found by qRT-PCR in ectopic endometriosis lesions. In an in vivo mouse model with human endometrial explants from patients with endometriosis, 10 μg MIA-602 per day resulted in significantly smaller human endometrial xenotransplants after 4 weeks compared to mice treated with vehicle. The endometrial tissues expressed SV1 before and after xenotransplantation. The proliferation of endometrial stromal cells as well as the endometriosis cell lines 12-Z and 49-Z was decreased by exposure to 1 μM MIA-602 after 72 hours. The protein levels of epithelial growth factor receptors in 12-Z and 49-Z cell lines were reduced 48 and 72 hours after the administration of 1 μM MIA-602. MIA-602 decreased the activation of the MAP-kinases ERK-1/2. Our study demonstrates the presence of SV1 receptor as a target for treatment with GHRH antagonist in endometriosis. Endometrial tissues respond to MIA-602 with inhibition of proliferation in vitro and in vivo. The use of MIA-602 could be an effective supplement to the treatment strategies in endometriosis.

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Transplacental Transfer of a Growth Hormone-Releasing Hormone Peptide from Mother to Fetus in the Rat

Cited by 7 publications

References 43 publications

Effects of Plasmid Growth Hormone–Releasing Hormone Treatment during Heat Stress

Effects of Plasmid Growth Hormone–Releasing Hormone Treatment during Heat Stress

The growth hormone–insulin-like growth factor axis in pregnancy

Effects of an Antagonistic Analog of Growth Hormone-Releasing Hormone on Endometriosis in a Mouse Model and In Vitro

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