Trophoblast differentiation during embryo implantation and formation of the maternal-fetal interface

Red-Horse, Kristy; Zhou, Yan; Genbačev, Olga; Prakobphol, Akraporn; Foulk, Russell A.; McMaster, Michael; Fisher, Susan J.

doi:10.1172/jci22991

Cited by 334 publications

(209 citation statements)

References 136 publications

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“…MTA1 and MTA3 are thought to be master regulators of the EMT, an important diVerentiation mechanism of the human placenta (Vicovac and Aplin 1996;Red-Horse et al 2004). Therefore, although an expression of these proteins in human placental tissue could be theoretically suggested, it is quite interesting to demonstrate a signiWcant expression of both MTA1 and MTA3, since MTA3 is known to be repressed by MTA1 (Fujita et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…After implantation of the embryo into the maternal uterine wall, cells from the trophoectoderm layer of the blastocyst invade into the uterine stroma and maternal blood vessels, Wnally forming a feto-maternal tissue generally known as the placenta (Burrows et al 1996;Red-Horse et al 2004). Invasion into connective tissues, transmigration through blood vessels, and the capability of neoangiogenesis are characteristics of this process but likewise known as hallmarks of cancer progression (Hanahan and Weinberg 2000).…”

Section: Introductionmentioning

confidence: 99%

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The metastasis-associated genes MTA1 and MTA3 are abundantly expressed in human placenta and chorionic carcinoma cells

Brüning

Makovitzky

Gingelmaier

et al. 2009

Histochem Cell Biol

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Normal placenta development relies on the ability of trophoblast cells to invade into the uterus and to build up an extensively vascularized feto-maternal tissue, necessary for the nutrition of the embryo. The ability of cell migration, invasion, and the ability to induce neovascularization are likewise hallmarks of cancer cells. The metastasis-associated genes MTA1 and MTA3 are known to be involved in cancer cell migration by regulation of cell adhesion proteins and to induce the expression of neoangiogenic cytokines, as recently shown by us for ovarian cancer cells. Therefore, we analyzed the expression of MTA1 and MTA3 in normal human placenta tissues and the chorionic cancer cell lines BeWo, JEG, and JAR. Immunohistochemical analysis revealed a rather strong expression of MTA1 and MTA3 in the nuclei of human trophoblast cells. A high expression level of MTA1 and MTA3 was further observed in the nuclei of human chorionic carcinoma cells, as shown by immunofluorescence analysis, and confirmed by Western blot and RT-PCR analysis. We conclude that the high expression level of MTA proteins in human chorionic cells might facilitate trophoblast cell migration and neoangiogenesis, and might further predispose human chorionic cancer cells with properties that are characteristic for this highly aggressive and metastatic carcinoma type.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The metastasis-associated genes MTA1 and MTA3 are abundantly expressed in human placenta and chorionic carcinoma cells

Brüning

Makovitzky

Gingelmaier

et al. 2009

Histochem Cell Biol

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“…The extent of CTB differentiation to an invasive phenotype was assessed at a molecular level by evaluating cell expression of integrin α1 and HLA-G, stage-specific antigens upregulated during cell invasion of the uterine wall (Red-Horse et al 2004). In both cases, the coexpression of CK was used to confirm CTB identity.…”

Section: Assessment Of Ctb Differentiationmentioning

confidence: 99%

Comparative analysis of maternal-fetal interface in preeclampsia and preterm labor

et al. 2007

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The maternal-fetal interface, a chimeric structure, is formed when fetal cytotrophoblasts (CTBs) from the placenta invade the uterine wall and its resident vasculature. In preeclampsia (PE), interstitial and endovascular invasion are often shallow, and fewer spiral arterioles are breached in toto. Our previous work has shown that faulty CTB differentiation to an invasive phenotype is a contributing factor. Here, we have tested the hypothesis that the constellation of morphological and molecular defects that are associated with PE are unique to this condition. Specifically, we have compared the histology of the maternal-fetal interface and CTB expression of stage-specific antigens in PE and in preterm labor (PTL) with or without inflammation. In the absence of inflammation, biopsies obtained after PTL were near normal at histological and molecular levels. In accord with previously published data, PE had severe negative effects on the endpoints analyzed. Biopsies obtained after PTL with inflammation had an intermediate phenotype. Our results suggest that the maternal-fetal interface from cases of PTL without inflammation can be used for comparative purposes, e.g., as age-matched controls, in studies of the effects of PE on cells in this region.

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“…With its extensive villous or tree-like projections, it forms a direct link between mother and fetus [1][2][3]. On the surface of placental villi, a layer of multinucleated syncytiotrophoblasts in direct contact with maternal blood is essential for continuously supplying essential gases and nutrients to the developing fetus and removing metabolic waste.…”

Section: Introductionmentioning

confidence: 99%

“…The multinucleated syncytiotrophoblast layer is maintained by a continuous fusion of proliferated cytotrophoblasts during pregnancy. The aged syncytiotrophoblast cells are replaced by younger populations of trophoblasts without affecting neighboring cells [2,3]. The older material in the syncytiotrophoblast layer is then packed into a syncytial knot/ sprout, undergoes apoptosis, and sheds into maternal circulation [2][3][4].…”

Section: Introductionmentioning

confidence: 99%

Mammalian Ste20-like protein kinase 3 mediates trophoblast apoptosis in spontaneous delivery

Lin

Lin³

et al. 2007

Apoptosis

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The placenta is essential in transferring gases and nutrients from the mother to the developing fetus. Trophoblast apoptosis may cause labor or other pregnancy-related disorders. This study demonstrated the essential role of Mst3, a human Ste20-like protein kinase, in the oxidative stress-induced apoptosis of trophoblasts of term placenta in normal spontaneous delivery. Oxidative stress, but not hormones released during labor such as prostaglandin E1, oxytocin or angiotensin II, induces the expression of Mst3 and apoptosis of human term placenta after elective Cesarean section without labor pain. The role of Mst3 in oxidative stress-induced apoptosis was further demonstrated in the 3A-sub-E, a human trophoblast cell line. The H2O2-induced apoptosis of 3A-sub-E cells was largely suppressed by overexpressed Mst3KR, the kinase-dead mutant or by selective knockdown of endogenous Mst3. Further studies showed that Jun N-terminal kinase (JNK) may participate in the signaling pathway of H2O2-induced apoptosis by mediating the level of Mst3. Subsequently, caspase 3 and other downstream apoptotic components may be activated by Mst3 and trigger the apoptotic process in human trophoblasts.

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Trophoblast differentiation during embryo implantation and formation of the maternal-fetal interface

Cited by 334 publications

References 136 publications

The metastasis-associated genes MTA1 and MTA3 are abundantly expressed in human placenta and chorionic carcinoma cells

The metastasis-associated genes MTA1 and MTA3 are abundantly expressed in human placenta and chorionic carcinoma cells

Comparative analysis of maternal-fetal interface in preeclampsia and preterm labor

Mammalian Ste20-like protein kinase 3 mediates trophoblast apoptosis in spontaneous delivery

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