Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

Sado, Toshiyuki; Naruse, Katsuhiko; Noguchi, Taketoshi; Shoji, Hirokazu; Yoshida, Shozo; Tanase, Yasuhito; Kitanaka, Takashi; Oi, Hidekazu; Kobayashi, Hiroshi

doi:10.1007/s00011-011-0319-4

Cited by 26 publications

(26 citation statements)

References 83 publications

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“…13) As expected from previously reported serum concentrations, 15) our current study strongly suggests that hypoxia and reoxygenation in the preeclamptic placenta contributes to systemic release of the danger signal HMGB1. Cellular debris (microparticles) from syncytiotrophoblasts is regarded as a possible mediator of the systemic inflammation that connects placentation failure in the first trimester to later onset of preeclampsia; HMGB1 and S100 family members are considered candidate functional surface antigen molecules on the microparticles.…”

Section: )supporting

confidence: 87%

“…11,12) After reviewing the literature, we hypothesized that the inflammatory response induced in normal pregnancy, preeclampsia, and preterm birth may be regulated by changes in RAGE ligands. 13,14) We subsequently reported increased serum levels of two soluble RAGE ligands in preeclampsia patients, high-mobility group box 1 (HMGB1) and S100/calgranulin family member S100A12 (also known as extracellular newly identified RAGE-binding protein). 15) HMGB1 expression has also been reported in human term placenta.…”

Section: Introductionmentioning

confidence: 99%

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Cytokines, proteases, and ligands of receptor for advanced glycation endproducts (RAGE) released by primary trophoblasts from human term placenta under hypoxic stimulation

Naruse

Tsunemi

Onogi

et al. 2013

Hypertens Res Pregnancy

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Aim:In the placenta, hypoxia followed by reoxygenation (ischemia and reperfusion) is regarded as a trigger for the pathological onset of preeclampsia. In this study, we isolated primary trophoblasts from human term placenta, exposed them to hypoxic stress, and measured subsequent levels of cytokines, proteases, protease inhibitors, and ligands of receptor for advanced glycation endproducts (RAGE) to identify the trigger molecule released from hypoxic placenta into maternal circulation. Methods: Ten placental samples were taken from healthy elective caesarean section patients. Trophoblasts were isolated using a Percoll-based method and cultured under 20% oxygen with or without 3 rounds of 0.1% hypoxic stimulation for 1 h. Results: Cell viability did not differ between normal and hypoxic cultures (MTT assay), but cell injury was attenuated in hypoxic culture (LDH assay). In cell culture supernatants, concentrations of MMP-2, TIMP-2, IL-6, and IL-10 decreased in hypoxia compared to normal culture, while the RAGE ligand HMGB1 increased significantly in hypoxic culture. There were no significant differences in concentrations of MMP-9, TIMP-1, IL-8, or S100A12. Conclusions: These results suggest that human term placenta under hypoxia and reperfusion releases the RAGE ligand HMGB1, a "danger signal", that can trigger systemic inflammation and lead to preeclampsia or placenta-based complications in pregnancy.

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Section: )supporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Cytokines, proteases, and ligands of receptor for advanced glycation endproducts (RAGE) released by primary trophoblasts from human term placenta under hypoxic stimulation

Naruse

Tsunemi

Onogi

et al. 2013

Hypertens Res Pregnancy

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“…Higher methylation was also observed in some genes in the preeclampsia (Jia et al 2012). Here, we showed that the differentially expressed genes in preeclampsia placental tissues were mainly enriched in several pathways associated with pregnancy maintenance, metabolism, oxidative stress and oxidative metabolism, cell cycle regulation, embryogenesis and development, implantation, placentation and decidualization, immune modulation, and vascular function (Zhou et al 2006;Laivuori 2007;Founds et al 2009;Johansson et al 2011;Løset et al 2011;Rajakumar et al 2011;Sado et al 2011;Tsai et al 2011;Jia et al 2012;Lapaire et al 2012). We summarized the major functional categories on the differential gene expression profile between preeclampsia and normal placentas ( Table 1).…”

Section: Preeclampsia Susceptibility Genesmentioning

confidence: 83%

“…This review provides a detailed overview of typical genome-wide studies that have been conducted so far on preeclamptic placental tissue samples (Zhou et al 2006;Laivuori 2007;Founds et al 2009;Johansson et al 2011;Løset et al 2011;Rajakumar et al 2011;Sado et al 2011;Tsai et al 2011;Jia et al 2012;Lapaire et al 2012).…”

Section: Review Of the Literaturementioning

confidence: 99%

The Impact of Maternal-Fetal Genetic Conflict Situations on the Pathogenesis of Preeclampsia

Kobayashi

2015

Biochem Genet

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Preeclampsia leads to maternal and perinatal morbidity and mortality. The literature in English was reviewed to summarize recent advances in understanding the global gene expression changes in the pathogenesis of preeclampsia. We identified at least eight consistently enriched categories, relating to pregnancy maintenance, metabolism, oxidative stress, cell cycle regulation, implantation, decidualization, immune modulation, and vascular function. Expression profiling in preeclampsia placenta and normal placenta revealed 140 transcripts that were significantly differentially expressed, 30 (21.4%) of which were evolved for the protection of the mother, approximately three times less than the number of genes evolved for the benefit of the fetus [110 genes (78.6%)] in preeclampsia placenta versus normal placenta. The genome-wide analysis emphasizes the dysfunctional decidualization as the main mechanism involved in the development of preeclampsia. These genetic signaling events may occur from an imbalance in the maternal-fetal genetic response in the affected placenta. This is to our knowledge the first report on the pathogenesis of preeclampsia, in which preeclampsia may occur as a genetic consequence of maternal-fetal conflict situations during the early decidualization process.

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“…Pathways related to stress, inflammation (including TLR signalling pathways), growth, tissue remodelling, and metabolism are all altered during preeclampsia (Sado, Naruse et al 2011). The differences might reflect acute inflammation secondary to microbial infection versus chronic inflammation secondary to oxidative stress.…”

Section: Prrs and Adverse Pregnancy Outcomesmentioning

confidence: 99%

Cytokines and the Innate Immune Response at the Materno-Fetal Interface

Bryant¹,

Thornton²

2012

Recent Advances in Research on the Human Placenta

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Inflammatory pattern recognition receptors and their ligands: factors contributing to the pathogenesis of preeclampsia

Abstract: This review summarizes recent advances in TLR- and RAGE-mediated signaling and the target molecules, and provides new insights into the pathogenesis of preeclampsia.

Cited by 26 publications

References 83 publications

Cytokines, proteases, and ligands of receptor for advanced glycation endproducts (RAGE) released by primary trophoblasts from human term placenta under hypoxic stimulation

Cytokines, proteases, and ligands of receptor for advanced glycation endproducts (RAGE) released by primary trophoblasts from human term placenta under hypoxic stimulation

The Impact of Maternal-Fetal Genetic Conflict Situations on the Pathogenesis of Preeclampsia

Cytokines and the Innate Immune Response at the Materno-Fetal Interface

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