Decreased Levels of Folate Receptor‐β and Reduced Numbers of Fetal Macrophages (<scp>H</scp>ofbauer Cells) in Placentas from Pregnancies with Severe Pre‐Eclampsia

Tang, Zhonghua; Buhimschi, Irina A.; Buhimschi, Catalin S.; Tadesse, Serkalem; Norwitz, Errol R.; Niven‐Fairchild, Tracy; Huang, Su-Cheng; Guller, Seth

doi:10.1111/aji.12112

Cited by 51 publications

(59 citation statements)

References 72 publications

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“…FGR was defined as weight < 10th percentile for gestational age at birth in pregnancies not complicated by preeclampsia. A detailed description of these patients was previously reported [39–41]. …”

Section: Methodsmentioning

confidence: 99%

H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction

Zuckerwise

et al. 2016

Oncotarget

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Fetal growth restriction (FGR) is a well-recognized risk factor for perinatal mortality and morbidity, as well as neurodevelopmental impairment and adulthood onset disorders. Here we report that the H19 long noncoding RNA (lncRNA) is significantly decreased in placentae from pregnancies with FGR. Downregulation of H19 leads to reduced migration and invasion of extravillous trophoblast (EVT) cells in vitro. This is consistent with reduced trophoblast invasion that has been observed in FGR. Genome-scale transcriptome profiling of EVT cells reveals significantly decreased expression of the type III TGF-β receptor (TβR3) following H19 knockdown. Decreased TβR3 expression is also seen in FGR placentae. TβR3 repression decreases EVT cell migration and invasion, owing to impaired TGF-β signaling through a non-canonical TGF-β signaling pathway. Further, we identify TβR3 as a novel regulatory target of microRNA let-7. We propose that dysregulation of this newly identified H19/TβR3-mediated regulatory pathway may contribute to the molecular mechanism of FGR. Our findings are the first to show a lncRNA-based mechanism of FGR, holding promise for the development of novel predictive, diagnostic, and therapeutic modalities for FGR.

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Section: Methodsmentioning

confidence: 99%

H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction

Zuckerwise

et al. 2016

Oncotarget

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“…29 Conversely, we documented reduced HBC numbers in pregnancies with preeclampsia (PE). 30 Adverse neonatal outcomes including cerebral palsy are associated with preterm birth and HCA when accompanied by fetal inflammatory response syndrome (FIRS, a multisystemic microbial invasion of the fetus with the hallmark presentation of funisitis). [31][32][33] In situ RT-PCR revealed an infectious agent was present in 46 of the 60 placentas from newborns with respiratory distress and severe neurological sequelae.…”

Section: The Role Of Hofbauer Cells and Evidence For Their Microbiamentioning

confidence: 99%

Zika virus infection of Hofbauer cells

Simoni

Jurado

Abrahams

et al. 2016

American J Rep Immunol

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Recent studies have linked antenatalinfection with Zika virus (ZIKV) with major adverse fetal and neonatal outcomes, including microcephaly. There is a growing consensus for the existence of a congenital Zika syndrome (CZS). Previous studies have indicated that non-placental macrophages play a key role in the replication of Dengue virus (DENV), a closely related flavivirus. Since the placenta provides the conduit for vertical transmission of certain viruses, and placental Hofbauer cells (HBCs) are fetal-placental macrophages located adjacent to fetal capillaries, it is not surprising that several recent studies have examined infection of HBCs by ZIKV. In this review we describe congenital abnormalities associated with ZIKV infection, the role of HBCs in the placental response to infection, and evidence for the susceptibility of HBCs to ZIKV infection. We conclude that HBCs may contribute to the spread of ZIKV in placenta and promote vertical transmission of ZIKV, ultimately compromising fetal and neonatal development and function. Current evidence strongly suggests that further studies are warranted to dissect the specific molecular mechanism through which ZIKV infects HBCs and its potential impact on the development of CZS.

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“…Abnormal quantity of M1/M2 macrophages may result in PE . It is reported that PE is associated with a change in phenotype and function toward the M1/proinflammatory macrophage continuum . However, the reason why macrophages polarization changed in PE is unknown.…”

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confidence: 99%

TGF‐β3‐induced miR‐494 inhibits macrophage polarization via suppressing PGE2 secretion in mesenchymal stem cells

Zhao

Miao

et al. 2016

FEBS Letters

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Abnormal macrophage polarization at the maternal-fetal interface may contribute to the development of Preeclampsia (PE). The reason why macrophage polarization changed in PE is still unclear. Decidual mesenchymal stem cells (dMSCs) could regulate macrophage polarization. However, miRNA in dMSCs of PE were maladjusted. Therefore, we speculated that miRNA may affect dMSC-regulated macrophage polarization. In this study, we found that miR-494-overexpressed dMSCs inhibit M2 macrophage polarization and this inhibitory effect is mediated by miR-494-reduced PGE2 secretion. Furthermore, we proved that miR-494 is induced by TGF-b3. In summary, our findings suggest that the high expression of TGF-b3 in PE decidua stimulates miR-494 in dMSCs and attenuates the regulation of MSC switching the macrophage toward M2 type, contributing to an immune imbalance at maternal-fetal interface.

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Decreased Levels of Folate Receptor‐β and Reduced Numbers of Fetal Macrophages (Hofbauer Cells) in Placentas from Pregnancies with Severe Pre‐Eclampsia

Cited by 51 publications

References 72 publications

H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction

H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction

Zika virus infection of Hofbauer cells

TGF‐β3‐induced miR‐494 inhibits macrophage polarization via suppressing PGE2 secretion in mesenchymal stem cells

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