Models for Study of Human Embryo Implantation: Choice of Cell Lines?1

Hannan, Natalie J.; Paiva, Premila; Dimitriadis, Evdokia; Salamonsen, Lois A.

doi:10.1095/biolreprod.109.077800

Cited by 266 publications

(207 citation statements)

References 150 publications

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“…Experimental results arising from primary human cells freshly isolated may better reflect human biology than immortalized cell lines that have likely undergone multiple passages. 33 Furthermore, primary cells provide better models for preeclampsia in vitro. 34 However, a potential limitation of our study is that we isolated primary trophoblast cells from term placentas.…”

Section: Discussionmentioning

confidence: 99%

Sofalcone Upregulates the Nuclear Factor (Erythroid-Derived 2)–Like 2/Heme Oxygenase-1 Pathway, Reduces Soluble fms–Like Tyrosine Kinase-1, and Quenches Endothelial Dysfunction

et al. 2015

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P reeclampsia is a pregnancy specific condition affecting ≈5% to 8% of all pregnancy in women and a leading cause of maternal and perinatal morbidity and mortality.1 An imbalance between angiogenic and antiangiogenic factors leading to endothelial dysfunction is proposed to be a key mechanism of preeclampsia. Previous landmark studies identified that antiangiogenic factors, such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), play crucial roles in the development of preeclampsia.2,3 Administration of both sFlt-1 and sEng causes severe preeclamptic phenotype in rodents. Furthermore, sFlt-1 and sEng have also been shown to have predictive significance in clinic in women who go onto to develop preeclampsia. 4Heme oxygenase-1 (HO-1) is an inducible rate-limiting enzyme, which catalyzes free heme into carbon monoxide, free iron, and biliverdin. It is known that HO-1-derived carbon monoxide and biliverdin have strong anti-inflammatory and antioxidant properties.5 Transcription of HO-1 mRNA is Abstract-Preeclampsia is a severe complication of pregnancy, characterized by hypertension, oxidative stress, and severe endothelial dysfunction. Antiangiogenic factors, soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin, play key pathophysiological roles in preeclampsia. Heme oxygenase-1 (HO-1) is a cytoprotective, antioxidant enzyme reported to be downregulated in preeclampsia. Studies propose that inducing HO-1 may also decrease sFlt-1 production. Sofalcone, a gastric antiulcer agent in clinical use, is known to induce HO-1 in gastric epithelium. We aimed to investigate whether sofalcone induces HO-1 and reduces sFlt-1 release from primary human placental and endothelial cells and blocks endothelial dysfunction in vitro. We isolated human trophoblasts and endothelial cells (human umbilical vein endothelial cells) and also used uterine microvascular cells. We investigated the effects of sofalcone on (1) HO-1 production, (2) activation of the nuclear factor (erythroid-derived 2)-like 2 pathway, (3) sFlt-1 and soluble endoglin release, (4) tumor necrosis factor α-induced monocyte adhesion and vascular cell adhesion molecule upregulation, and (5) endothelial tubule formation. Sofalcone potently increased HO-1 mRNA and protein in both primary trophoblasts and human umbilical vein endothelial cells. Furthermore, sofalcone treatment caused nuclear translocation of nuclear factor (erythroid-derived 2)-like 2 and transactivation of other nuclear factor (erythroid-derived 2)-like 2 responsive genes (NQO1, TXN, and GCLC). Importantly, sofalcone significantly decreased the secretion of sFlt-1 from primary human trophoblasts. Sofalcone potently suppressed endothelial dysfunction in 2 in vitro models, blocking tumor necrosis factor α-induced monocyte adhesion and vascular cell adhesion molecule 1 expression in human umbilical vein endothelial cells. These results indicate that in primary human tissues, sofalcone can potently activate antioxidant nuclear factor (erythroid-derived 2)-like 2/HO-1 pathw...

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Section: Discussionmentioning

confidence: 99%

Sofalcone Upregulates the Nuclear Factor (Erythroid-Derived 2)–Like 2/Heme Oxygenase-1 Pathway, Reduces Soluble fms–Like Tyrosine Kinase-1, and Quenches Endothelial Dysfunction

et al. 2015

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“…68 Having monolayer cell culture model have their own limitations as we have evidenced that paracrine signals are involved in leading the endometrium to the matured state. Using intact endometrial strips in vivo cultures were not successful as they lead to necrotic changes at the center of the tissue.…”

Section: Models To Study Embryo Implantationmentioning

confidence: 99%

Endometrial Receptivity and Human Embryo Implantation

Rashid

Lalitkumar

et al. 2011

American J Rep Immunol

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Citation Rashid NA, Lalitkumar S, Lalitkumar PG, Gemzell‐Danielsson K. Endometrial Receptivity and Human Embryo Implantation. Am J Reprod Immunol 2011; 66 (Suppl. 1): 23–30Problem The pre‐requisite of successful implantation involves an intricate cascade of molecular interactions which plays a crucial role in preparing receptive endometrium and implanting blastocyst.Method of study Data are hereby presented for a better understanding of endometrial receptivity in women, hoping to provide a comprehensive picture of the process and identify new areas of basic and translational research in the biology of blastocyst implantation.Results Timely regulation of the expression of a number of complex molecules like hormones, cytokines and growth factors, and their crosstalk from embryonic and maternal endometrial side play a major role in determining the fate of the embryo. The molecular basis of endometrial receptivity and the mechanisms by which the blastocyst first adheres to the luminal epithelium and then penetrates into the stroma are only just beginning to be resolved.Conclusion Advances in the development of implantation models and ‘omics’ technologies, particularly proteomics and metabolomics, are set to have a major impact on the development of this field.

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“…Neither of the available trophoblast cell lines [18] represent the physiological conditions since these are either choriocarcinomaderived (e.g., JEG-3, BeWo, JAR) or immortalized by transformation of human extravillous trophoblast cells with the SV40 large T antigen (e.g., HTR-8/SVneo, SGHPL-4, HIPEC65).…”

Section: Introductionmentioning

confidence: 99%

Progesterone-induced blocking factor differentially regulates trophoblast and tumor invasion by altering matrix metalloproteinase activity

Halász

Polgar

Berta

et al. 2013

Cell. Mol. Life Sci.

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Invasiveness is a common feature of trophoblast and tumours; however, while tumour invasion is uncontrolled, trophoblast invasion is strictly regulated. Both trophoblast and tumour cells express high levels of the immunomodulatory Progesterone-Induced Blocking Factor (PIBF), therefore, we aimed to test the possibility that PIBF might be involved in invasion. To this aim we used PIBF silenced or PIBF treated trophoblast (HTR8/Svneo, and primary trophoblast) and tumour (HT-1080, A549, HCT116, PC3) cell lines. Silencing of PIBF increased invasiveness as well as MMP-2,-9 secretion of HTR8/SVneo, and decreased those of HT-1080 cells. PIBF induced immediate STAT6 activation in both cell lines. Silencing of IL-4Rα abrogated all the above effects of PIBF, suggesting that invasion-related signalling by PIBF is initiated through the IL-4Rα/PIBF-receptor complex. In HTR-8/SVneo PIBF induced fast, but transient Akt and ERK phosphorylation, whereas in tumour cells PIBF triggered sustained Akt, ERK and late STAT3 activation. The late signalling events might be due to indirect action of PIBF. PIBF induced the expression of EGF and HB-EGF in HT-1080 cells. The STAT3 activating effect of PIBF was reduced in HB-EGF deficient HT-1080 cells, suggesting that PIBF-induced HB-EGF contributes to late STAT3 activation. PIBF binds to the promoters of IL-6, EGF and HB-EGF; however, the protein profile of the protein/DNA complex is different in the two cell lines. We conclude that in tumour cells PIBF induces proteins, which activate invasion signalling, while -based on our previous data -PIBF might control trophoblast invasion by suppressing invasive genes.

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Models for Study of Human Embryo Implantation: Choice of Cell Lines?1

Cited by 266 publications

References 150 publications

Sofalcone Upregulates the Nuclear Factor (Erythroid-Derived 2)–Like 2/Heme Oxygenase-1 Pathway, Reduces Soluble fms–Like Tyrosine Kinase-1, and Quenches Endothelial Dysfunction

Sofalcone Upregulates the Nuclear Factor (Erythroid-Derived 2)–Like 2/Heme Oxygenase-1 Pathway, Reduces Soluble fms–Like Tyrosine Kinase-1, and Quenches Endothelial Dysfunction

Endometrial Receptivity and Human Embryo Implantation

Progesterone-induced blocking factor differentially regulates trophoblast and tumor invasion by altering matrix metalloproteinase activity

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