Placental function in development and disease

Cross, James C.

doi:10.1071/rd05121

Cited by 112 publications

(77 citation statements)

References 74 publications

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“…Both human and rodent placentas consist of analogous cell types that are involved in placental transport processes [3][4][5][6][7][8][9][10][11]. In rodents, the placenta comprises two zones: the junctional zone and the labyrinth.…”

Section: Introductionmentioning

confidence: 99%

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Id2 Mediates Differentiation of Labyrinthine Placental Progenitor Cell Line, SM10

Selesniemi

Albers

Brown

2016

Stem Cells and Development

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The placenta is an organ that is formed transiently during pregnancy, and appropriate placental development is necessary for fetal survival and growth. Proper differentiation of the labyrinthine layer of the placenta is especially crucial, as it establishes the fetal-maternal interface that is involved in physiological exchange processes. Although previous studies have indicated the importance of inhibitor of differentiation/inhibitor of DNA binding-2 (Id2) helix-loop-helix transcriptional regulator in mediating cell differentiation, the ability of Id2 to regulate differentiation toward the labyrinthine (transport) lineage of the placenta has yet to be determined. In the current study, we have generated labyrinthine trophoblast progenitor cells with increased (SM10-Id2) or decreased (SM10-Id2-shRNA) Id2 expression and determined the effect on TGF-b-induced differentiation. Our Id2 overexpression and knockdown analyses indicate that Id2 mediates TGF-b-induced morphological differentiation of labyrinthine trophoblast cells, as Id2 overexpression prevents differentiation and Id2 knockdown results in differentiation. Thus, our data indicate that Id2 is an important molecular mediator of labyrinthine trophoblast differentiation. An understanding of the regulators of trophoblast progenitor differentiation toward the labyrinthine lineage may offer insights into events governing pregnancy-associated disorders, such as placental insufficiency, fetal growth restriction, and preeclampsia.

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Section: Introductionmentioning

confidence: 99%

“…Trophoblast cells that make up the placenta must properly differentiate into the appropriate cell types (lineages) to facilitate this transport [3][4][5][6][7]. Abnormal placental development has been proposed to lead to a reduction in placental function and subsequent pregnancyassociated disorders [1][2][3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Id2 Mediates Differentiation of Labyrinthine Placental Progenitor Cell Line, SM10

Selesniemi

Albers

Brown

2016

Stem Cells and Development

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“…The placenta is a major endocrine gland that also regulates the maternal-fetal flow of nutrients and waste (Cross 2006). Aberrant placental development may result in fetal defects, as well as gestational trophoblast diseases, such as choriocarcinoma (Cheung 2003).…”

Section: Introductionmentioning

confidence: 99%

Changes in cell cycle and extracellular matrix gene expression during placental development in deer mouse (Peromyscus) hybrids

Duselis

Obergfell

Mack

et al. 2007

Reprod. Fertil. Dev.

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Abstract.Crosses between two species of the rodent genus Peromyscus produce defects in both growth and development. The defects are pronounced in the hybrid placentas. Peromyscuys maniculatus (strain BW) females mated to P. polionotus (strain PO) males produce placentas half the size of the parental species, as well as growth-retarded embryos. In contrast, PO females mated to BW males result in defective conceptuses that display embryonic and placental overgrowth. These 'parent-of-origin'-dependent phenotypes are consistent with previous studies that demonstrated altered expression of imprinted genes and genetic linkage of the overgrowth phenotypes to imprinted domains. In the present study, we take a broader approach in assessing perturbations in hybrid placental gene expression through the use of Mus musculus cDNA microarrays. In verifying classes of genes identified in microarray screens differentially regulated during hybrid placental development, we focused on those influencing the cell cycle and extracellular matrix (ECM). Our work suggests that cell cycle regulators at the G 1 /S phase check-point are downregulated in the large hybrid placenta, whereas the small hybrid placenta is more variable. The ECM genes are typically downstream targets of cell cycle regulation and their misregulation is consistent with many of the dysmorphic phenotypes. Thus, these data suggest imbalances in proliferation and differentiation in hybrid placentation.

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“…15 Failure of EVT invasion can lead to intrauterine growth restriction and preeclampsia. 16,17 Preeclampsia, a pregnancy-specific disorder characterized by hypertension and proteinuria, is a major cause of maternal and fetal morbidity and mortality. 18 Defects in placentation, particularly trophoblast invasion, are thought to contribute to the onset of this disorder.…”

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confidence: 99%

Nodal Signals through Activin Receptor-Like Kinase 7 to Inhibit Trophoblast Migration and Invasion

Nadeem

Munir

et al. 2011

The American Journal of Pathology

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Trophoblast cell invasion into the uterus is an essential process for successful pregnancy, and shallow invasion of trophoblasts into the maternal decidua is linked to preeclampsia. We have reported that Nodal, a member of the transforming growth factor-␤ superfamily, acts through activin receptor-like kinase 7 (ALK7) to inhibit trophoblast proliferation and to induce apoptosis. In this study, we examined the spatial and temporal expression patterns of Nodal and ALK7 in human placenta from normal and preeclamptic pregnancies and investigated whether Nodal regulated trophoblast migration and invasion. Nodal and ALK7 were detected in villous and extravillous trophoblast cell populations in early gestation, and their levels were strongly up-regulated in preeclamptic placenta. Overexpression of Nodal or constitutively active ALK7 decreased cell migration and invasion, whereas knockdown of Nodal and ALK7 had the opposite effects. In placental explant culture, treatment with Nodal inhibited trophoblast outgrowth, whereas Nodal small-interfering RNA strongly induced the expansion of explants and the migration of extravillous trophoblast cells. Nodal stimulated the secretion of tissue inhibitor of metalloproteinase-1 and inhibited matrix metalloproteinase (MMP)-2 and MMP-9 activity. These findings suggest that the Nodal/ALK7 pathway plays important roles in human placentation and that its abnormal signaling may contribute to the development of preeclampsia.

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Placental function in development and disease

Cited by 112 publications

References 74 publications

Id2 Mediates Differentiation of Labyrinthine Placental Progenitor Cell Line, SM10

Id2 Mediates Differentiation of Labyrinthine Placental Progenitor Cell Line, SM10

Changes in cell cycle and extracellular matrix gene expression during placental development in deer mouse (Peromyscus) hybrids

Nodal Signals through Activin Receptor-Like Kinase 7 to Inhibit Trophoblast Migration and Invasion

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