Trophoblast-specific transcription from the mouse placental lactogen-I gene promoter.

Shida, Miho M.; Ng, Yuk Kiu; Soares, Michael J.; Linzer, Daniel I. H.

doi:10.1210/mend.7.2.8469232

Cited by 24 publications

(5 citation statements)

References 20 publications

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“…To confirm the suppressive effect of the HOP/NECC1-SRF pathway on Pl1 expression, we performed Pl1 reporter assays using luciferase vector, which contains the critical promoter region for Pl1 (11). After 72 h of spontaneous differentiation, as expected, Pl1 luciferase activity increased to 3.9 times higher than that under stem cell conditions (Fig.…”

Section: Resultssupporting

confidence: 55%

HOP/NECC1, A Novel Regulator of Mouse Trophoblast Differentiation

Asanoma

Kato

Yamaguchi

et al. 2007

Journal of Biological Chemistry

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Homeodomain-only protein/not expressed in choriocarcinoma clone 1 (HOP/NECC1) is a newly identified gene that modifies the expression of cardiac-specific genes and thereby regulates heart development. More recently, HOP/NECC1 was reported to be a suppressor of choriocarcinogenesis. Here, we examined the temporal expression profile of HOP/NECC1 in wild-type mouse placenta. We found that E8.5-E9.5 wild-type placenta expressed HOP/NECC1 in the giant cell and spongiotrophoblast layers. HOP/NECC1 (؊/؊) placenta exhibited marked propagation of giant cell layers and, in turn reduction of spongiotrophoblast formation. We demonstrated SRF transcriptional activity increased in the differentiating trophoblasts and forced expression of SRF in a trophoblast stem (TS) cell line induces the differentiation into giant cells. Negative regulation of SRF (serum response factor) by the binding of HOP/NECC1 protein contributed at least in part to the generation of these placental defects. Gradual induction of HOP/NECC1 in response to differentiation stimuli may result in the decision to differentiate into a particular type of trophoblastic cell lineage and result in non-lethal defects shown by the HOP/NECC1 (؊/؊) placentas.The development of the placenta starts with differentiation of the outer layer of the blastocyst, the trophectoderm. After implantation, the mural trophectodermal cells contribute to primary trophoblast giant (TG) 2 cells and the polar trophectoderm differentiates to extraembryonic ectoderm (ExE). ExE grows to form the ectoplacental cone (EPC), which contains precursor cells that give rise to spongiotrophoblasts (SpT) and secondary TG cells. Most TG cells originate from precursor cells located in the EPC, and partially from SpT (1). The TG cells are polyploid as a result of endoreduplication (repeated rounds of DNA synthesis without cell division) (2, 3).In the course of exploring the molecular mechanism of gestational trophoblastic diseases, we have isolated a candidate choriocarcinoma suppressor gene (NECC1, not expressed in choriocarcinoma clone 1) (4). Normal placental villi express NECC1 but choriocarcinoma cell lines and tissue samples fail to express it. We transfected the NECC1 gene into choriocarcinoma cell lines to characterize its functions as a tumor suppressor gene and observed remarkable alterations in cell morphology (4).This unusual type of homeodomain protein also functions during cardiac development. Genetic inactivation of the mouse orthologue HOP (homeodomain-only protein) results in a partially penetrant phenotype of embryonic heart failure and lethality (5, 6). HOP/NECC1-deficient adult mice display conduction defects (7). HOP/NECC1 contains a unique homeodomain that is incapable of sequence-specific DNA binding (5, 6). Instead, HOP/NECC1 functions by interacting with SRF to inhibit DNA binding by recruiting histone deacetylase (HDAC) activity (8). This interaction results in decreased transcription of SRF-dependent cardiomyocyte-specific genes (5, 6).The fact that HOP/NECC1 is expressed in h...

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Section: Resultssupporting

confidence: 55%

HOP/NECC1, A Novel Regulator of Mouse Trophoblast Differentiation

Asanoma

Kato

Yamaguchi

et al. 2007

Journal of Biological Chemistry

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“…Initially, the expression of endogenous prl3d1 in various tissues of C57BL/6JGpt mice was determined by qRT–PCR. As shown in Figure 1a, the prl3d1 mRNA was mainly expressed in the placenta tissues, which consistent with previous reports (Shida et al, 1993). Prl3d1 exhibited weak expression in the liver, lung, spleen, kidney, stomach, intestine, embryo and testis tissues, while being scarcely detectable in the heart (Figure 1a).…”

Section: Resultssupporting

confidence: 92%

“…Embryos were stained with DAPI and visualized and photographed with an LSM700 confocal microscope (Zeiss, Germany). tissues, which consistent with previous reports (Shida et al, 1993).…”

Section: In Vitro Fertilization Assaysupporting

confidence: 94%

The Prl3d1‐Cre mouse line selectively induces the expression of Cre recombinase in parietal trophoblast giant cells

Pan,

Zhu,

et al. 2023

Genesis

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SummaryThe placenta plays a pivotal role in the maintenance of normal pregnancy, but how it forms, matures, and performs its function remains poorly understood. Here, we describe a novel mouse line (Prl3d1‐iCre) that expresses iCre recombinase under the control of the endogenous prl3d1 promoter. Prl3d1 has been proposed as a marker for distinguishing trophoblast giant cells (TGCs) from other trophoblast cells in the placenta. The in vivo efficiency and specificity of the Cre line were analyzed by interbreeding Prl3d1‐iCre mice with B6‐G/R reporter mice. Through anatomical studies of the placenta and other tissues of Prl3d1‐iCre/+; B6‐G/R mouse mice, we found that the tdTomato signal was expressed in parietal trophoblast giant cells (P‐TGCs). Thus, we report a mouse line with ectopic Cre expression in P‐TGCs, which provides a valuable tool for studying human pathological pregnancies caused by implantation failure or abnormal trophoblast secretion due to aberrant gene regulation.

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“…Despite a broad knowledge concerning genes which harbor AP‐1 binding sites in their regulatory elements, only a few directly regulated AP‐1 target genes have been identified. Among the most well‐characterized AP‐1 regulated genes are c‐ jun itself and genes involved in tissue remodeling processes such as proteinases, including MMP‐9 (gelatinase B; Reponen et al ., 1995; Alexander et al ., 1996), uPA (Nerlov et al ., 1992; De Cesare et al ., 1995) and their inhibitors, as well as the placental hormones placental lactogen‐I (PL‐I) (Carney et al ., 1993; Shida et al ., 1993) and proliferin (Carney et al ., 1993; Groskopf and Linzer, 1994).…”

Section: Introductionmentioning

confidence: 99%

JunB is essential for mammalian placentation

Schorpp-Kistner

Wang

Angel

et al. 1999

EMBO J

242

189

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Lack of JunB, an immediate early gene product and member of the AP-1 transcription factor family causes embryonic lethality between E8.5 and E10.0. Although mutant embryos are severely retarded in growth and development, cellular proliferation is apparently not impaired. Retardation and embryonic death are caused by the inability of JunB-deficient embryos to establish proper vascular interactions with the maternal circulation due to multiple defects in extra-embryonic tissues. The onset of the phenotypic defects correlates well with high expression of junB in wild-type extra-embryonic tissues. In trophoblasts, the lack of JunB causes a deregulation of proliferin, matrix metalloproteinase-9 (MMP-9) and urokinase plasminogen activator (uPA) gene expression, resulting in a defective neovascularization of the decidua. As a result of downregulation of the VEGF-receptor 1 (flt-1), blood vessels in the yolk sac mesoderm appeared dilated. Mutant embryos which escape these initial defects finally die from a nonvascularized placental labyrinth. Injection of junB -/-embryonic stem (ES) cells into tetraploid wild-type blastocysts resulted in a partial rescue, in which the ES cell-derived fetuses were no longer growth retarded and displayed a normal placental labyrinth. Therefore, JunB appears to be involved in multiple signaling pathways regulating genes involved in the establishment of a proper feto-maternal circulatory system.

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Trophoblast-specific transcription from the mouse placental lactogen-I gene promoter.

Cited by 24 publications

References 20 publications

HOP/NECC1, A Novel Regulator of Mouse Trophoblast Differentiation

HOP/NECC1, A Novel Regulator of Mouse Trophoblast Differentiation

The Prl3d1‐Cre mouse line selectively induces the expression of Cre recombinase in parietal trophoblast giant cells

JunB is essential for mammalian placentation

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