CURRENT TOPIC: To Be, or Not to Be, That is the Question. Apoptosis in Human Trophoblast

Levy, Rivka; Nelson, D. Michael

doi:10.1053/plac.1999.0450

Cited by 116 publications

(51 citation statements)

References 106 publications

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“…Apoptosis of villous trophoblast in situ or apoptosis of nucleated fetal cells circulating in maternal blood may also lead to release of fetal DNA into the maternal circulation. 8,9 The successful prevention of RhD disease has brought attention to other red blood cells' antigens including RhC/c and RhE/e. The presence of RhE/e and RhC/c antibodies causing alloimmunisation was shown to be 14% and 10.7%, respectively, in an upstate New York female population with RhD still being the leading antigen at 21%.…”

Section: Introductionmentioning

confidence: 99%

Noninvasive fetal RhCE genotyping from maternal blood

Geifman-Holtzman

Grotegut

Gaughan

et al. 2008

BJOG

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Background The successful prevention of RhD disease has brought attention to other red blood cells' antigens causing alloimmunisation including RhC/c and RhE/e. Prenatal diagnosis of fetal Rh genotype from maternal blood is in clinical use in Europe but not in the USA.Objective To estimate the collective reported diagnostic accuracy of fetal RhCE genotyping from peripheral maternal blood and compare the results of genotyping when fetal cells and free fetal DNA (FfDNA) are used.Search strategy English-written literature describing fetal RhCE determination from maternal blood using fetal cells or FfDNA was performed using medical subject headings and text words. The sources included Pubmed (1966Pubmed ( -2007, Ovid , CINAHL, The Cochrane Library, ACP Journal Club and OCLC. Key words were prenatal diagnosis, fetal RhCE, fetal DNA in maternal blood and alloimmunisation.Selection criteria A study was considered eligible if it described fetal RhCE type determination using maternal peripheral blood reported in the English literature. Abstracts were excluded.Data collection and analysis From each study, we determined the number of samples tested, fetal RhCE genotype, the source of the fetal DNA, gestational age, presence of alloimmunisation and confirmation of fetal RhCE type. Exclusions and inclusions were noted. We calculated composite estimates of accuracy using a weighted random effects model. We assessed the papers against an international quality, STARD checklist which is standards for reporting studies of diagnostic accuracy.Main results We identified 20 protocols in six English-written publications reporting fetal RhC/c (seven protocols) and/or E/e (13 protocols) genotyping using DNA obtained from maternal blood for a total of 369 samples. For RhC/c, 176 samples were tested and for RhE/e, 193 samples were tested. Accuracy was determined for each study and for all studies. The combined accuracy of fetal genotype was 96.3% for RhC/c and 98.2% for RhE/e. Only a few samples of the sorted cells were found to be a source for accurate diagnosis, but plasma was consistently the best source of fetal RhCE genotyping in 147/147 (100%) for RhC/c and 168/168 (100%) for RhE/e.Conclusions The combined accuracy of noninvasive fetal RhC/c or RhE/e determination using maternal peripheral blood is 96.3% and 98.2%, respectively. FfDNA in maternal plasma is a better source for genotyping reported to be 100% correct for both RHCE genotypes. Further studies and reports of accuracy from laboratories performing the tests are required before prenatal determination of fetal RhC/c or RhE/e genotypes from maternal blood can safely replace the current methods used in the management of the RhC/c or RhE alloimmunised pregnancies.

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Section: Introductionmentioning

confidence: 99%

Noninvasive fetal RhCE genotyping from maternal blood

Geifman-Holtzman

Grotegut

Gaughan

et al. 2008

BJOG

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“…[1][2][3] These cellular events are closely linked and likely regulated by many of the same molecules.…”

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confidence: 99%

Mtd/Bok takes a swing: proapoptotic Mtd/Bok regulates trophoblast cell proliferation during human placental development and in preeclampsia

et al. 2009

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We have previously reported that matador/Bcl-2 ovarian killer (Mtd/Bok), a proapoptotic member of the Bcl-2 family, regulates human trophoblast apoptosis and that its levels are elevated in severe preeclamptic pregnancy. Herein, we show that Mtd is also involved in the regulation of proliferation in normal and pathological placentae. Mtd was found in proliferating trophoblast cells during early placental development and in preeclampsia (PE). The main isoform of Mtd associated with trophoblast proliferation was Mtd-L, the full-length isoform, which preferentially localized to the nuclear compartment in proliferating cells, whereas during apoptosis it switched localization to the cytoplasm where it associated with mitochondria. Mtd expression in proliferating cells colocalized with cyclin E1, a G 1 /S phase cell cycle regulator. MtdL-specific knockdown in the early first trimester villous explants and in HEK293 revealed a direct effect of Mtd-L on cyclin E1 expression and cell cycle progression. We conclude that Mtd-L functions to regulate trophoblast cell proliferation during early placentation and that the elevated levels of Mtd found in PE may contribute to increased trophoblast proliferation accompanying this devastating disorder of pregnancy.

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“…Here, the trophoblastic choriocarcinoma cell line, JAr, showed a better survival following hypoxia than 293HEK cells, an embryonic kidney cell line (data not shown). Programmed cell death plays a pivotal role in maintaining placental development and function throughout gestation (7,35). But even here, the border between 'good' and 'bad' apoptosis has to be drawn tightly as it is known that preeclampsia is linked to an increased rate of apoptotic death within trophoblasts (8 -10).…”

Section: Discussionmentioning

confidence: 99%

“…Trophoblasts are responsible for the maternalfetal exchange of gas, nutrients and waste products. Therefore, placental apoptosis is a key cellular interface in the control of placental homeostasis (7). Several authors have provided evidence for a connection between pathological states during pregnancy (e.g.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-induced leptin production in human trophoblasts does not protect from apoptosis

et al. 2005

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Objective: The ob-gene product, leptin, is an important regulator of placental and fetal development during pregnancy. Leptin, being induced by hypoxia in the placenta, is a known pro-apoptotic molecule in adipose tissue but is also known to inhibit apoptosis in other tissues like neuroblastoma cells. Based on these findings, we investigated if leptin has a pro-or anti-apoptotic effect on a trophoblastic cell line (JAr cells) in the presence or absence of oxygen. Methods and results: Measurement of leptin in the supernatant by using ELISA showed hypoxiainduced leptin production in JAr cells in vitro. This could be confirmed by a leptin-specific RT-PCR. By analyzing leptin and/or hypoxia exposed cells with FACS cytometry we found that JAr cells can cope with hypoxia down to oxygen tensions of 1%. At this level, only a small number of cells underwent apoptosis. Interestingly, leptin added to the culture medium in high concentrations was not able to interfere with the rate of proliferation or apoptosis in these cells independent of the oxygen tension. Finally, an anti-caspase-3 and anti-caspase-9 Western blot was performed. Again, no difference in the expression of caspase-3 and -9 under the conditions tested was seen. Conclusions: These results show that leptin, produced by placental cells after hypoxia in vitro, has no influence on the rate of proliferation of these cells. Furthermore, it does not influence apoptotic pathways in the trophoblastic cell line tested under hypoxic and non-hypoxic conditions. European Journal of Endocrinology 153 455-461

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CURRENT TOPIC: To Be, or Not to Be, That is the Question. Apoptosis in Human Trophoblast

Cited by 116 publications

References 106 publications

Noninvasive fetal RhCE genotyping from maternal blood

Noninvasive fetal RhCE genotyping from maternal blood

Mtd/Bok takes a swing: proapoptotic Mtd/Bok regulates trophoblast cell proliferation during human placental development and in preeclampsia

Hypoxia-induced leptin production in human trophoblasts does not protect from apoptosis

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