Ontogeny of Growth Hormone Releasing Hormone and Insulin-Like Growth Factors-I and-II Messenger RNA in Rat Placenta

Pescovitz, Ora Hirsch; Johnson, Nancy; Berry, Susan A.

doi:10.1203/00006450-199105010-00019

Cited by 21 publications

(9 citation statements)

References 29 publications

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“…The present Northern analysis data indicate that mGHRF mRNA is expressed as early as Day 11 of pregnancy in the mouse placenta and that its steady-state levels reach peak values on Days 15-17. This gestational profile, showing a marked increase in GHRF mRNA levels during the second half of pregnancy, is very similar to that reported for GHRF mRNA in the rat placenta [4], with the exception that rat GHRF mRNA was detected at very low levels as early as Day 6 of pregnancy by dot blot hybridization. It is likely that the apparent absence of GHRF mRNA in the mouse placenta prior to midpregnancy reflects a difficulty in detecting very low levels of mRNA rather than a true species difference between mice and rats in the ontogeny of placental GHRF.…”

Section: Discussionsupporting

confidence: 76%

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Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Endo

Yamaguchi

Farnsworth

et al. 1994

Biology of Reproduction

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The initial objective of this study was to establish a placental cell culture system in which the secretion of mouse growth hormone-releasing factor (mGHRF) could be examined during a several-day period. To determine when during pregnancy placental cells begin to express mGHRF, Northern blot analysis was carried out on total RNA from placentas collected on Days 6, 9, 11, 13, 15, 17, and 18 of pregnancy. Mouse GHRF mRNA could be detected as early as Day 11 of pregnancy. Its steady-state levels increased to maximum values on Days 15-17 and then declined slightly on Day 18. Placentas from Day 12 of pregnancy were selected for cell culture. The basal zone and labyrinth were dispersed in collagenase, and the cells were fractionated on a Percoll gradient. Two bands of cells were selected for further study. Both released significant amounts of immunoreactive mGHRF during a 5-day culture period. Effects of prolonged exposure of the cells to 8-bromo-cAMP and to agents that elevate intracellular cAMP concentration were then examined. Treatment of the cells with 0.5 mM 8-bromo-cAMP resulted in a significant decrease in the mGHRF concentration of the medium by the second day of culture. Mouse GHRF secretion was also inhibited by treatment of the cells with 100 ng/ml cholera toxin or 0.1 mM forskolin. The effect of 8-bromo-cAMP was concentration-dependent, with 0.1 mM being the lowest concentration that was active. 8-Bromo-cAMP treatment also reduced the steady-state level of mGHRF mRNA in the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 76%

“…One of these is growth hormone (GH)-releasing factor (GHRF). Both GHRF mRNA and peptide have been identified in the rat placenta [1][2][3][4][5], and GHRF mRNA has been identified in the mouse placenta [6,7]. There is some evidence for the expression of GHRF in the human placenta as well [8].…”

Section: Introductionmentioning

confidence: 95%

Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Endo

Yamaguchi

Farnsworth

et al. 1994

Biology of Reproduction

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“…transcripts increase during late pregnancy (Gray et al, 1987;Pescovitz et al, 1991). It remains unclear whether retarded fetal growth in the IGF-I1 gene disruption model is secondary to decreased IGF-I1 in the fetus, placenta, or both.…”

Section: Introductionmentioning

confidence: 99%

Differential expression of insulin‐like growth factor‐II in specific regions of the late (post day 9.5) murine placenta

Redline

Chernicky

Tan

et al. 1993

Molecular Reproduction Devel

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Insulin-like growth factor-II (IGF-II) expression has been implicated as a major determinant of fetal size during murine pregnancy. It remains unclear whether expression in the fetus, the placenta, or both is the overriding factor controlling growth. To gain further understanding of the placental contribution, we mapped IGF-II expression in the fetal vascular and trophoblastic portions of the late murine placenta (day 9.5-18.5). We found that, as in the fetus itself, vasculogenic mesenchyme, in this case derived from the allantois, was the strongest expressor of IGF-II. Trophoblast, on the other hand, while expressing somewhat less IGF-II, showed a dynamic pattern of IGF-II expression, which reflected its continuing differentiation during late pregnancy. Initially (days 9.5 and 12.5), the spongiotrophoblast, which is homologous to the cytotrophoblast columns and shell in early human pregnancy, strongly expressed IGF-II. Later, expression in the spongiotrophoblast was down-regulated as a new population, the so-called glycogen cells, emerged within the spongiotrophoblast (day 12.5-15.5) and went on to invade the mesometrial decidua. Glycogen cells, which are homologous to human intermediate trophoblast, strongly expressed IGF-II. Trophoblast lining the area of maternal-fetal exchange, the labyrinth, on the other hand, maintained a constitutive lower level of IGF-II expression throughout late pregnancy.

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“…These physiological states are characterized by highly coordinated changes in endometrial and myometrial mRNA expression of insulin-like growth factors (IGFs), IGF receptors and IGF binding proteins (IGFBPs) -the IGF system. In the uterus of several species, including the pig and rat, IGF-I mRNAs predominate in early pregnancy, whereas IGF-II mRNA accumulation occurs primarily after implantation (Letcher et al 1989, Pescovitz et al 1991, Simmen et al 1992, suggesting that these mitogens have either distinct or overlapping actions at the embryo-maternal and feto-maternal interfaces, respectively. The high peri-implantation expression of the IGF-I gene in porcine uterus coincides temporally with increased uterine luminal fluid IGF-I content (Simmen et al 1989), elongation of spherical blastocysts to the filamentous morphology (Geisert et al 1982), and transient conceptus secretion of estrogens (Gadsby et al 1980, Pusateri et al 1990, Green et al 1995, which are paracrine regulators of endometrial function, possibly in concert with endometrial-synthesized IGF-I.…”

Section: Introductionmentioning

confidence: 99%

Complex mediation of uterine endometrial epithelial cell growth by insulin-like growth factor-II (IGF-II) and IGF-binding protein-2

Badinga¹,

Song²,

Simmen³

et al. 1999

Journal of Molecular Endocrinology

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The coexpression of IGF (-I and -II) peptides, corresponding receptors, and IGF binding proteins (IGFBPs) in uterine endometrium suggests that a significant component of IGF action in this tissue is via autocrine or paracrine pathways, or both. The present study examined whether IGF-II and a major uterine-expressed IGF-II binding protein, IGFBP-2, modulate endometrial epithelial cell mitogenesis. Serum-deprived porcine endometrial glandular epithelial (GE) cells of early pregnancy were treated with various concentrations of IGFs, recombinant porcine (rp) IGFBP-2, or both, and examined for changes in cellular mitogenesis by incorporation of [ ]-IGF-II or rhIGF-II stimulated thymidine incorporation to a greater extent than did rhIGF-I alone. Ligand blot analysis of GE cell conditioned medium revealed the presence of four IGFBPs with molecular masses of 48, 31, 23, and 15 kDa. Physiological concentrations of rpIGFBP-2 (nM range) increased both basal and IGF-induced DNA synthesis in GE cells. At equimolar concentrations, Des(1-6)IGF-II (an IGF-II analog with much reduced affinity for IGFBPs) and rpIGFBP-2 had additive effects on GE cell mitogenesis, suggesting that the IGFBP-2 modulation of uterine cell growth may involve both IGF-dependent and IGF-independent pathways. Our results demonstrate the complex interplay of IGF system components in uterine endometrial epithelial growth regulation in vitro, identify IGF-II and IGFBP-2 as locally coexpressed uterine epithelial cell mitogens, and suggest the presence of a functional signaling pathway by which IGF-II stimulates epithelial cell proliferation via the type II receptor.

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Ontogeny of Growth Hormone Releasing Hormone and Insulin-Like Growth Factors-I and-II Messenger RNA in Rat Placenta

Cited by 21 publications

References 29 publications

Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Differential expression of insulin‐like growth factor‐II in specific regions of the late (post day 9.5) murine placenta

Complex mediation of uterine endometrial epithelial cell growth by insulin-like growth factor-II (IGF-II) and IGF-binding protein-2

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