Cytogenetic and DNA-Fingerprint Characterization of Choriocarcinoma Cell Lines and a Trophoblast /Choriocarcinoma Cell Hybrid

Frank, Hans-Georg; Gunawan, Bastian; Ebeling-Stark, Ingke; Schulten, Hans-Juergen; Funayama, Hitoshi; Cremer, Ulrich; Huppertz, Berthold; Gaus, Gabriele; Kaufmann, Peter; Füzesi, L.

doi:10.1016/s0165-4608(99)00107-7

Cited by 46 publications

(24 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Primary extravillous trophoblast cells are of only limited value for in vitro induction of apoptosis because they spontaneously undergo apoptosis shortly after isolation . Therefore, we employed a hybrid cell line, generated by hybridization of extravillous trophoblast cells with choriocarcinoma cells (Frank et al, 2000), to address our hypothesis. Different from their choriocarcinoma parent cells (see the control experiments Ia and IIe), these trophoblast hybrid cells respond to proapoptotic stimuli in vitro as normal extravillous trophoblast cells do in vivo (Huppertz et al, 1998a, and pilot data of this study).…”

Section: Discussionmentioning

confidence: 99%

“…Extravillous trophoblast was not studied. We decided to employ immortalized extravillous trophoblast cells generated by hybridization with choriocarcinoma cells (Frank et al, 2000) …”

Section: The Apoptosis-inducing Effects Of Exogenous Tnf␣ On Trophoblmentioning

confidence: 99%

“…These hybrid cells exhibited many phenotypic similarities to extravillous trophoblast (Frank et al, 2000), including the expression of TNF-RI. Our in vitro data demonstrate that exogenous TNF␣ induces apoptosis in extravillous trophoblast hybrid cells.…”

Section: Reister Et Almentioning

confidence: 99%

“…At present, no cell line fulfills all the criteria necessary to be considered extravillous trophoblast (King et al, 2000). The monoclonal choriocarcinoma/extravillous trophoblast hybrid cell line, AC-1M59 (Frank et al, 2000), shares many features with invasive extravillous trophoblast. Among others, it is cytokeratin-positive, exhibits an invasive phenotype in vitro (G. Desoye, University of Graz, personal communication, 2001), and expresses HLA-G (A.…”

Section: Choriocarcinoma/extravillous Trophoblast Hybrid Cells As a Mmentioning

confidence: 99%

See 3 more Smart Citations

Macrophage-Induced Apoptosis Limits Endovascular Trophoblast Invasion in the Uterine Wall of Preeclamptic Women

Reister

Frank

Kingdom

et al. 2001

Laboratory Investigation

Self Cite

272

167

View full text Add to dashboard Cite

SUMMARY:Impaired invasion of uteroplacental arteries by extravillous trophoblast cells is a key pathogenic mechanism of preeclampsia. We previously demonstrated that reduced trophoblast invasion into uteroplacental spiral arteries was associated with an excess of macrophages in and around these arteries. To explore the significance of these observations, we correlated the extent of extravillous trophoblast apoptosis in placental bed biopsy specimens with macrophage distribution and studied the effect of macrophages upon trophoblast apoptosis in vitro. Extravillous trophoblast hybrid cells were cocultured with activated macrophages exposed to exogenous tumor necrosis factor ␣ (TNF␣), anti-tumor necrosis factor receptor I (TNF-RI), and tryptophan depletion, and the rates of trophoblast apoptosis were measured. Extravillous trophoblast hybrid cells showed increased rates of apoptosis following exposure to exogenous TNF␣, with tryptophan depletion, and when cocultured with activated macrophages. The proapoptotic effects of macrophages in vitro were completely inhibited only by simultaneous addition of tryptophan and anti-TNF-RI. Our data indicate that macrophages, residing in excess in the placental bed of preeclamptic women, are able to limit extravillous trophoblast invasion of spiral arterial segments through apoptosis mediated by the combination of TNF␣ secretion and tryptophan depletion. The mechanisms by which macrophages are activated and recruited to the placental bed are presently unknown but are likely central to the pathogenesis of preeclampsia. (Lab Invest 2001,

show abstract

Section: Discussionmentioning

confidence: 99%

“…Extravillous trophoblast was not studied. We decided to employ immortalized extravillous trophoblast cells generated by hybridization with choriocarcinoma cells (Frank et al, 2000) …”

Section: The Apoptosis-inducing Effects Of Exogenous Tnf␣ On Trophoblmentioning

confidence: 99%

Section: Reister Et Almentioning

confidence: 99%

Section: Choriocarcinoma/extravillous Trophoblast Hybrid Cells As a Mmentioning

confidence: 99%

See 2 more Smart Citations

Macrophage-Induced Apoptosis Limits Endovascular Trophoblast Invasion in the Uterine Wall of Preeclamptic Women

Reister

Frank

Kingdom

et al. 2001

Laboratory Investigation

Self Cite

272

167

View full text Add to dashboard Cite

show abstract

“…The cell lines AC1M-32 [19] and ACH-3P [20] have been generated by fusion of the AC1-1 cell line (a JEG-3 mutant [21]) with primary term or first trimester trophoblasts, respectively. In addition, trophoblast cell lines such as HTR-8/SVneo [22] and SGHPL-5 [23] have been generated by SV40 large T antigen transfection.…”

Section: Introductionmentioning

confidence: 99%

Toll-like receptor profiling of seven trophoblast cell lines warrants caution for translation to primary trophoblasts

et al. 2015

View full text Add to dashboard Cite

Expression of the imprinted genesMEST/Mest in human and murine placenta suggests a role in angiogenesis

et al. 2000

Self Cite

View full text Add to dashboard Cite

Cytogenetic and DNA-Fingerprint Characterization of Choriocarcinoma Cell Lines and a Trophoblast /Choriocarcinoma Cell Hybrid

Cited by 46 publications

References 20 publications

Macrophage-Induced Apoptosis Limits Endovascular Trophoblast Invasion in the Uterine Wall of Preeclamptic Women

Macrophage-Induced Apoptosis Limits Endovascular Trophoblast Invasion in the Uterine Wall of Preeclamptic Women

Toll-like receptor profiling of seven trophoblast cell lines warrants caution for translation to primary trophoblasts

Expression of the imprinted genesMEST/Mest in human and murine placenta suggests a role in angiogenesis

Contact Info

Product

Resources

About