Elevated expression of KiSS-1 in placenta of preeclampsia and its effect on trophoblast

Zhang, Hong; Long, Qifang; L, Li; Gao, Aihua; Li, Huifen; Lin, Qi

doi:10.1016/s1642-431x(12)60048-5

Cited by 39 publications

(34 citation statements)

References 22 publications

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“…Despite kisspeptin-10 being the most potent physiological inhibitor of trophoblast invasion in the placenta [16], most preeclampsia studies have focused on the expression of different forms of kisspeptins ( Table 3). The finding of elevated kisspeptin expression in preeclamptic placentae concurs with those from previous studies [22,24]. In addition trophoblasts isolated from preeclamptic placentae exhibit increased Kiss-1 mRNA and metastin (kisspeptin-54) expression and this expression correlates positively with the severity of disease [20].…”

Section: Discussionsupporting

confidence: 90%

“…In contrast the placental expression of both Kiss-1 and GPR-54 transcripts are highest in the first trimester (when control of invading trophoblasts is most crucial) and lowest at term [16,19]. Several studies have reported elevated Kiss-1 mRNA and protein expression in trophoblasts [20] and placentae of pregnancies complicated by preeclampsia [21][22][23][24]. Cartwright and Williams (2012) reported increased kisspeptin receptor expression in preeclamptic placentae [21], while Qiao et al (2012) found no difference in placental Kiss-1R mRNA and protein expression between healthy and preeclamptic pregnancies [22].…”

Section: Introductionmentioning

confidence: 99%

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Elevated placental expression at the maternal–fetal interface but diminished maternal circulatory kisspeptin in preeclamptic pregnancies

Matjila

Millar

Spuy

et al. 2016

Pregnancy Hypertension: An International Journal of Women's Car

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Elevated placental expression at the maternal–fetal interface but diminished maternal circulatory kisspeptin in preeclamptic pregnancies

Matjila

Millar

Spuy

et al. 2016

Pregnancy Hypertension: An International Journal of Women's Car

View full text Add to dashboard Cite

“…In this study, the development of preeclampsia was found to be associated with deregulation in the levels of H3K9/27me3, showing increased levels of H3K9me3 and both H3K9/27me3 associated with low expression of MMP2 and MMP9 respectively. These results support the documented deficient expression of MMP2 and MMP9, in preeclampsia (Lockwood et al 2008, Zhang et al 2011. MMPs also play important role in controlling the bioactivity of growth factors, angiogenic factors, cytokines (Staun-Ram & Shalev 2005), and release of VEGF (Monaco et al 2006), thus their deficient expression in preeclampsia might also be hampering the VEGF release, as supported by lower levels of VEGF reported in preeclampsia (Levine et al 2004).…”

Section: Discussionsupporting

confidence: 81%

Imbalance between matrix metalloproteinases and their tissue inhibitors in preeclampsia and gestational trophoblastic diseases

Rahat¹,

Sharma²,

Bagga³

et al. 2016

Reproduction

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The invasion cascade exhibited by placental trophoblasts and cancerous cells bears many similarities, and it is attributed to extracellular matrix degradation mediated by matrix metalloproteinases (MMPs). Although proper and controlled invasion by trophoblasts into the maternal uterus is an essential requirement for maintenance of normal pregnancy, any abnormality in this phenomenon results in the development of invasion-related disorders such as gestational trophoblastic diseases (GTDs) and preeclampsia. We studied the epigenetic basis of differential expression of two placental MMPs (MMP2 and MMP9) and tissue inhibitors of metalloproteinases (TIMP2 and TIMP1) during normal gestation and invasion-related disorders, i.e., preeclampsia and GTDs. Our study suggests the association of H3K9/27me3 with differential expression of these MMPs and their inhibitors, which regulate the placental invasion during normal pregnancy, whereas no role of CpG methylation was observed in the differential expression of MMPs/TIMPs. Further, development of GTDs was associated with abnormally higher expression of these MMPs and lower levels of their inhibitors, whereas the reverse trends were observed for MMPs and their TIMPs in case of preeclampsia, in association with abnormal changes in H3K9/27me3. These results suggest the involvement of higher levels of MMPs in an aggressive invasive behavior depicted by GTDs, whereas lower levels of these MMPs in shallow and poor invasive phenotype associated with preeclampsia. Thus, our study shows the significance of a proper balance regulated by histone trimethylation between differential expression of MMPs and their TIMPs for maintaining normal pregnancy and its deregulation as a contributing factor for pathogenesis of invasive disorders during pregnancy.

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“…Similar to what is reported in other cases of shallow trophoblast invasion (e.g. pre-eclampsia), (Sood et al 2006;Lian et al 2010;Mayor-Lynn et al 2011;Zhang et al 2011), we expected that MMP2 and MMP9 would be expressed in isolated canine trophoblasts and canine placental tissues. Using RT-PCR, Lei et al (2007) reported an upregulation in MMP9 expression that was associated with differentiation of mouse trophoblast stem cells expected to occur at the end of pregnancy.…”

Section: Discussionsupporting

confidence: 79%

Who Let the Dogs In: A Canine Trophoblast Invasion Model for Pre‐eclampsia

Kutzler

Sahlfeld

Fellows

2012

Reprod Domestic Animals

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ContentsPre-eclampsia affects 2-8% of pregnant women worldwide and is the third leading cause of maternal mortality in the United States, accounting for 20% of maternal deaths, for which the only known cure is delivery of the placenta. It is known that pre-eclampsia results from defects within the trophoblast invasion of the endometrium and myometrium. At a morphological level within the pre-eclamptic human placenta, trophoblast invasion is shallow, and this results in hypoperfusion, which is a life-threatening condition for both the mother and the foetus. Pre-eclampsia has been intensively investigated for over 50 years, and yet the causes are largely unknown. Despite a large body of data, it is still unknown exactly which mechanisms regulate trophoblast invasion. An effective animal model may be crucial to understanding the underlying causes of pre-eclampsia. A canine model is a proposed improvement on the current efforts to investigate disorders of shallow trophoblast invasion throughout gestation and to improve understanding of the factors that regulate trophoblast invasion. The objectives of this research were to elucidate and compare cellular and molecular similarities between normal canine trophoblasts with those from recently published reports on pre-eclampsia in women.

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Elevated expression of KiSS-1 in placenta of preeclampsia and its effect on trophoblast

Cited by 39 publications

References 22 publications

Elevated placental expression at the maternal–fetal interface but diminished maternal circulatory kisspeptin in preeclamptic pregnancies

Elevated placental expression at the maternal–fetal interface but diminished maternal circulatory kisspeptin in preeclamptic pregnancies

Imbalance between matrix metalloproteinases and their tissue inhibitors in preeclampsia and gestational trophoblastic diseases

Who Let the Dogs In: A Canine Trophoblast Invasion Model for Pre‐eclampsia

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