Placental-specific expression from the mouse placental lactogen II gene promoter.

Shida, Miho M.; Jackson-Grusby, Laurie; Ross, Susan R.; Linzer, Daniel I. H.

doi:10.1073/pnas.89.9.3864

Cited by 50 publications

(23 citation statements)

References 34 publications

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“…Reverse transcription polymerase chain reaction analyses were performed to determine the relationship between expression of PECs and markers of trophoblast giant cells during differentiation of these cells. PL-1, a glycopeptide hormone that is expressed by trophoblast giant cells, was elevated during differentiation, consistent with previous studies with these cells (fig1C) [25,26]. The basic helix-loop-helix transcription factors Hand1 and Stra13 showed a similar pattern of expression.…”

Section: Cathepsin P Expression Is Induced During Differentiation Of supporting

confidence: 78%

Expression of Cathepsin P mRNA, Protein and Activity in the Rat Choriocarcinoma Cell Line, Rcho-1, During Giant Cell Transformation

Hassanein

Korant

et al. 2007

Placenta

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Lysosomal proteases perform critical functions in protein turnover and are essential for normal growth and development. Cathepsin P is a member of a newly discovered family of lysosomal cysteine proteases uniquely expressed in rodent placenta (PECs), and is closely related to human cathepsin L. Using the rat choriocarcinoma cell line model, Rcho-1, mRNA for the PECs cathepsins P, M, Q, R, 1, 2 was found to increase in expression during differentiation into a trophoblast giant cell phenotype. By contrast, expression of cathepsin L was not regulated. A specific enzyme assay was developed to show that activity of cathepsin P mirrored mRNA expression during differentiation. Cathepsin P protein co-localizes with cathepsin B, indicating that the enzyme probably functions in the endosomal-lysosomal compartment. This study demonstrates that the PEC genes produce functional proteases that can perform specific placental roles that are probably performed by broader specificity proteases in human placenta.

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Section: Cathepsin P Expression Is Induced During Differentiation Of supporting

confidence: 78%

Expression of Cathepsin P mRNA, Protein and Activity in the Rat Choriocarcinoma Cell Line, Rcho-1, During Giant Cell Transformation

Hassanein

Korant

et al. 2007

Placenta

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“…The mPL-II-producing cells in cultures of day 7 placenta are larger than those in cultures of day 12 placenta, as assessed in the reverse hemolytic plaque assay and after immunohistochemical staining. It is likely that the smaller cells originate from the labyrinth zone, since cultures of day 12 placenta would be expected to contain relatively more cells from this region than would cultures from earlier days of pregnancy (31), and mPL-II has been localized by in situ hybridization (32,33) and immunohistochemical staining (ref. 34; M.Y., unpublished data) to this region.…”

Section: Discussionmentioning

confidence: 99%

Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro.

Yamaguchi¹,

Ógren²,

Southard³

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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The mouse placenta produces several polypeptides belonging to the prolactin-growth hormone gene family, including mouse placental lactogen (mPL) I and mPL-II. The present study was undertaken to determine whether the secretion of mPL-I and mPL-H is regulated by interleukin 6 (IL-6), which is present in the placenta and has previously been reported to stimulate the secretion of pituitary members of this gene family. Effects of human and mouse IL-6 on mPL-I and mPL-II secretion were examined in primary cultures of placental cells from days 7, 9, and 12 of pregnancy. IL-6 caused a dose-dependent reduction in the mPL-HI concentration in the medium of cells from days 9 and 12 of pregnancy but did not affect the mPL-II concentration in the medium ofcells from day 7 of pregnancy or the mPL-I concentration in the medium of cells from days 7 or 9 of pregnancy. The lowest concentration of human IL-6 that significantly inhibited mPL-II secretion was 250 pM. The effect of IL-6 on the mPL-II concentration in the medium was due primarily to inhibition of mPL-II synthesis, which resulted at least partly from a decrease in the steady-state level of mPL-II mRNA. These data raise the possibility that IL-6 may regulate mPL-I production after midpregnancy in vivo.

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“…Sections (10 to 12 m thick) were cut, allowed to dry, and either refrozen (at Ϫ80°C) or immediately processed for RNA in situ hybridization (16). RNA probes were generated as previously described: Cited1 (17), 4311 (Tpbp) (14), Mest (Peg1) (38), proliferin (PLF) (33), and mouse placental lactogen II (mPLII) (58). The sections were counterstained with eosin.…”

Section: Targeting Vectors and Generation Of The Cited1mentioning

confidence: 99%

Cited1 Is Required in Trophoblasts for Placental Development and for Embryo Growth and Survival

Rodríguez¹,

Sparrow²,

Scott³

et al. 2004

Molecular and Cellular Biology

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Cited1 is a transcriptional cofactor that interacts with Smad4, estrogen receptors ␣ and ␤, TFAP2, and CBP/p300. It is expressed in a restricted manner in the embryo as well as in extraembryonic tissues during embryonic development. In this study we report the engineering of a loss-of-function Cited1 mutation in the mouse. Cited1 null mutants show growth restriction at 18.5 days postcoitum, and most of them die shortly after birth. Half the heterozygous females, i.e., those that carry a paternally inherited wild-type Cited1 allele, are similarly affected. Cited1 is normally expressed in trophectoderm-derived cells of the placenta; however, in these heterozygous females, Cited1 is not expressed in these cells. This occurs because Cited1 is located on the X chromosome, and thus the wild-type Cited1 allele is not expressed because the paternal X chromosome is preferentially inactivated. Loss of Cited1 resulted in abnormal placental development. In mutants, the spongiotrophoblast layer is irregular in shape and enlarged while the labyrinthine layer is reduced in size. In addition, the blood spaces within the labyrinthine layer are disrupted; the maternal sinusoids are considerably larger in mutants, leading to a reduction in the surface area available for nutrient exchange. We conclude that Cited1 is required in trophoblasts for normal placental development and subsequently for embryo viability.

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Placental-specific expression from the mouse placental lactogen II gene promoter.

Abstract: The gene for mouse placental lactogen II

Cited by 50 publications

References 34 publications

Expression of Cathepsin P mRNA, Protein and Activity in the Rat Choriocarcinoma Cell Line, Rcho-1, During Giant Cell Transformation

Expression of Cathepsin P mRNA, Protein and Activity in the Rat Choriocarcinoma Cell Line, Rcho-1, During Giant Cell Transformation

Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro.

Cited1 Is Required in Trophoblasts for Placental Development and for Embryo Growth and Survival

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