Placental prolactin-like proteins in rodents: Variations on a structural theme

Southard, Jonathan N.; Talamantes, Frank

doi:10.1016/0303-7207(91)90084-6

Cited by 39 publications

(11 citation statements)

References 28 publications

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“…The typical interferon signaling pathway is activated through the JAK-STAT system [22]. It is well known that pituitary hormone GH and prolactin also activate the JAK-STAT system [23], and that several prolactin-like molecules including placental lactogen are abundantly produced in the placenta [24]. We can not exclude the possibility that, in addition to interferon-beta, the prolactin-like molecules produced in the placenta may also play significant roles in the induction of interferonregulated genes.…”

Section: Discussionmentioning

confidence: 88%

Identification of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-inducible and -suppressive Genes in the Rat Placenta: Induction of Interferon-regulated Genes with Possible Inhibitory Roles for Angiogenesis in the Placenta

et al. 2004

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Abstract. Exposure to a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in a variety of toxic manifestations, including fetal death. In order to evaluate the effects of low dose TCDD on placental function, pregnant Holtzman rats were given a single oral dose of 1600 ng TCDD/kg body wt or an equivalent volume of vehicle (control) on gestation day 15 (GD15), and changes in the gene expression in the placenta on GD20 were analyzed by two comprehensive methods, representational difference analysis (RDA) and DNA microarray technology. Candidates of TCDD-inducible and -suppressive genes were selected. Quantitative real-time PCR analysis was then performed to verify the induction or suppression levels of the candidate genes. Finally, we identified 81 TCDD-inducible and 21 TCDD-suppressive genes from the placenta of TCDD-treated Holtzman rats on GD20. One of the remarkable profiles of the gene expression was that glucose transporters were strongly up-regulated by the TCDD treatment. Furthermore, many interferon-inducible genes were also up-regulated by the treatment. They included several cytokines such as IP-10 known as a potent angiogenesis inhibitor. In addition, interferon molecules are known to suppress angiogenesis. The above observations suggest that activation of the interferon signaling pathway and the induction of anti-angiogenic factors by TCDD might have a role in causing the inhibition of neovascularization, resulting in the hypoxic state of placenta and increased incidence of fetal death.Key words: TCDD, Placenta, Gene expression, Real-time PCR, DNA microarray (Endocrine Journal 51: 569-577, 2004) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is known to be the most toxic congener among the dioxin and related compounds found in the environment. Exposure to TCDD causes a diverse spectrum of toxicities in humans and laboratory animals [1][2][3][4]. The fetus is one of the most sensitive targets of TCDD and exhibits a wide range of biological responses at low TCDD levels that have no detectable effects on maternal side (usually the levels were ten to hundred times lower than those of LD50). One of the most severe adverse effects of TCDD is intrauterine fetal death [1,[5][6][7]. The incidence has been shown in all species studied to date, including the monkey, hamster, rat, and mouse. Although fetal death is an important aspect of TCDD toxicity, its precise mechanism is not well understood. Placenta plays a crucial role in maintaining normal fetal growth such as exchange of oxygen and carbohydrate nutrients. In previous studies Ishimura et al.

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Section: Discussionmentioning

confidence: 88%

Identification of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-inducible and -suppressive Genes in the Rat Placenta: Induction of Interferon-regulated Genes with Possible Inhibitory Roles for Angiogenesis in the Placenta

et al. 2004

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“…This delection could bring together two a-helix segments predicted for rodent prolactin-like proteins [ 121. In addition, Cyss7 (Cys'* in the mature PLFs), which is a conserved residue among every member of the mouse GHI PRL family [12,23] would be absent in the translation product of sPLF mRNAs. This Cys residue seems to be involved in disulphide bonds in MPR/PLFs and other members of the family [23].…”

Section: Fraction Numbermentioning

confidence: 99%

“…In addition, Cyss7 (Cys'* in the mature PLFs), which is a conserved residue among every member of the mouse GHI PRL family [12,23] would be absent in the translation product of sPLF mRNAs. This Cys residue seems to be involved in disulphide bonds in MPR/PLFs and other members of the family [23]. These changes should lead to significant variations in the sPLF properties for macromolecular interaction with respect to other reported MRP/PLFs.…”

Section: Fraction Numbermentioning

confidence: 99%

Expression of different mitogen‐regulated protein/proliferin mRNAs in Ehrlich carcinoma cells

Gil‐Torregrosa¹,

Urdiales²,

Lozano³

et al. 1994

FEBS Letters

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Results from in vivo and from serum-free primary cultures of Ehrlich cells suggest that the expression of mitogen-regulated protein/proliferin (MRP/PLF) mRNAs is not essential for proliferation of this murine tumor. Two sizes for MRP/PRL-related open reading frames (ORFs) have been detected by reverse transcription/PCR amplification. They are almost identical to that reported for PLF-1; but 20% of the amplified cDNA included a shorter ORF, which lacks the entire sequence corresponding to that of the exon 3 of the mrplplfgenes. Ehrlich carcinoma may represent a good model to study regulation of expression and physiological roles of MRP/PLFs in vivo.

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“…[7][8][9][10][11][12]. Of these, the four Cys residues, which are considered to be parts of the disulfide bonds that determine the tertiary structure of proteins [24,25], are conserved in the rat PL family without exception. In addition, three other amino acids, Arg at 43 and 202 and Lys at 212 in PL-Im, have also been postulated to be essential for reactions with the lactogenic hormone receptor in a study of point mutation in mouse PLs [26,27].…”

Section: Discussionmentioning

confidence: 99%

A cDNA Encoding a New Member of the Rat Placental Lactogen Family, PL-I mosaic (PL-Im).

et al. 1994

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Abstract. We have isolated a cDNA encoding a novel placental lactogen (PL), PL-I mosaic (PL-Im), by screening the cDNA library in ,ZAP of the mid-pregnant (day 12) rat placenta. The cDNA comprised an open reading frame of 687 by encoding 229 amino acids, in which there were two putative Nglycosylation sites. Northern blot analysis showed that PL-Im mRNA was expressed specifically during mid-pregnancy (days 10 and 12) in the rat placenta. The cDNA was highly homologous with those of other rat PL family members; in particular, the homology among PL-Im, PL-I (mid-pregnancy-specific) and PL-Iv (late-pregnancy-specific) was over 90%. Interestingly, the nucleotide sequence of PL-Im cDNA was a mosaic of PL-I and PL-Iv and it did not possess its own particular sequence. As the genomic pattern determined using Southern blot analysis of PL-Im was distinct from that of PL-I and PLIv, the encoded area of PL-Im appears to be independent of those of PL-I and PL-Iv on the gene. In the dendrogram of the rat PL family constructed on the basis of the nucleotide sequence homologies, PL-Im was located between PL-Iv and PL-I in the process of molecular evolution. Therefore, PL-Im has a unique cDNA structure and may be a principal factor in the molecular evolution of PLs.

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Placental prolactin-like proteins in rodents: Variations on a structural theme

Cited by 39 publications

References 28 publications

Identification of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-inducible and -suppressive Genes in the Rat Placenta: Induction of Interferon-regulated Genes with Possible Inhibitory Roles for Angiogenesis in the Placenta

Identification of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-inducible and -suppressive Genes in the Rat Placenta: Induction of Interferon-regulated Genes with Possible Inhibitory Roles for Angiogenesis in the Placenta

Expression of different mitogen‐regulated protein/proliferin mRNAs in Ehrlich carcinoma cells

A cDNA Encoding a New Member of the Rat Placental Lactogen Family, PL-I mosaic (PL-Im).

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