Transcriptional effects of hypoxia on fusiogenic syncytin and its receptor ASCT2 in human cytotrophoblast BeWo cells and in ex vivo perfused placental cotyledons

Knerr, Ina; Weigel, Christiane; Linnemann, Knud; Dötsch, Jörg; Meißner, Udo; Fusch, Christoph; Rascher, Wolfgang

doi:10.1067/s0002-9378(03)00538-6

Cited by 37 publications

(32 citation statements)

References 18 publications

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“…Abnormal syncytin-1 expression and protein localization in human placenta may cause some diseases such as preeclampsia and HELLP (hemolysis, elevated liver enzymes and low platelets) during pregnancy [30][31][32][33]. Unfortunately, we can not research on these diseases directly in human body.…”

Section: Discussionmentioning

confidence: 99%

Syncytin-A Mediates the Formation of Syncytiotrophoblast Involved in Mouse Placental Development

Gong

Huang

Shi

et al. 2007

Cell Physiol Biochem

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Syncytin-A, a new mouse endogenous retroviral envelope protein expressed in placenta, can mediate cell fusion in vitro. But its physiological function was still unknown. We proposed a role for syncytin-A in syncytiotrophoblast (SynT) formation derived from the differentiation of trophoblast stem (TS) cells during placental development. To evaluate this hypothesis, we analyzed the involvement of syncytin-A in the differentiation of mouse TS cells. After withdrawing fibroblast growth factor 4 (FGF4), TS cells can fuse to form SynT cells. We found syncytin-A mRNA and protein expression are colinear with fusion index increase during TS cell differentiation. Expression of syncytin-A is localized in SynT cells through in situ immunofluorescent staining. By using specific antibody and antisense oligonucleotides, we demonstrated that inhibition of syncytin-A lead to obvious decrease of SynT cell formation. These results present evidence in support of the direct role for syncytin-A in mouse TS cell fusion and differentiation involved in placental development.

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Section: Discussionmentioning

confidence: 99%

Syncytin-A Mediates the Formation of Syncytiotrophoblast Involved in Mouse Placental Development

Gong

Huang

Shi

et al. 2007

Cell Physiol Biochem

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“…Hypoxic condition, which is one of the symptoms observed in preeclampsia (Redman 1991), downregulates ERVWE1 expression (Knerr et al 2003, Kudo et al 2003. However, molecular mechanism for the regulation of ERVWE1 expression has not been definitively characterized.…”

Section: Regulation Of Ervwe1 By Cd9mentioning

confidence: 99%

CD9 regulates transcription factor GCM1 and ERVWE1 expression through the cAMP/protein kinase A signaling pathway

Muroi¹,

Sakurai²,

Hanashi³

et al. 2009

Reproduction

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ERVWE1 (SYNCYTIN-1), a membrane protein originating from the envelope gene of human endogenous retrovirus-W (HERV-W), mediates the fusion of mononucleated cytotrophoblasts into multinucleated syncytiotrophoblast. Though ERVWE1 has been characterized since its discovery, regulatory mechanisms associated with ERVWE1 expression have not been firmly established. We hypothesized that membrane protein CD9, involved in cell-cell fusion of fertilization and myogenesis, could be involved in the regulation of ERVWE1 gene expression. In this study, regulatory mechanisms of ERVWE1 expression were studied using human choriocarcinoma BeWo cells. Forskolin is an activator of adenylate cyclase, which increased CD9 and ERVWE1 expression. The increase in CD9 expression was inhibited by a protein kinase A (PKA) inhibitor, Rp-cAMPS. These results indicate that CD9 expression is regulated by the cAMP/PKA signaling pathway. Overexpression of CD9 increased expression levels of ERVWE1 as well as GCM1 (hGCMa), which is a transcription factor known to activate ERVWE1 gene transcription. However, high ERVWE1 expression induced by CD9 overexpression did not result in the increase in chorionic gonadotropin, beta polypeptide production. Moreover, CD9-induced increase in ERVWE1 and GCM1 expressions were inhibited by Rp-cAMPS. These results suggest that CD9 increases GCM1 expression via the cAMP/PKA signaling pathway, resulting in the increase in ERVWE1 expression.

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“…36 In 2001 Lee and colleagues found evidence that preeclampsia is accompanied by a substantial reduction in syncytin expression and its dislocation from its normal position in the syncytial tissues, 43 observations that were confirmed by Knerr and colleagues. 44 Since the expression and function of syncytin are reduced by hypoxia, the disturbance seen in pre-eclampsia might be secondary to poor placental perfusion; 45 nevertheless, the same group suggests that pre-eclampsia may be viewed as an 'altered syncytin system'. 46 That the link between syncytin and preeclampsia is still far from resolved reflects the very complex and dynamic nature of the mechanics involved in the single best understood HERV mutualism.…”

Section: Hervs As Symbiontsmentioning

confidence: 99%

Human endogenous retroviruses in health and disease: a symbiotic perspective

Ryan

2004

JRSM

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Transcriptional effects of hypoxia on fusiogenic syncytin and its receptor ASCT2 in human cytotrophoblast BeWo cells and in ex vivo perfused placental cotyledons

Cited by 37 publications

References 18 publications

Syncytin-A Mediates the Formation of Syncytiotrophoblast Involved in Mouse Placental Development

Syncytin-A Mediates the Formation of Syncytiotrophoblast Involved in Mouse Placental Development

CD9 regulates transcription factor GCM1 and ERVWE1 expression through the cAMP/protein kinase A signaling pathway

Human endogenous retroviruses in health and disease: a symbiotic perspective

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