Expression of ACKR2 in placentas from different types of preeclampsia

Yan, Shujun; Cui, Shihong; Zhang, Linlin; Yang, Bo; Yuan, Yangyang; Lv, Xiaoyi; Han, Fei; Li, Yingying; Huang, Chenxi; Wang, Ping

doi:10.1016/j.placenta.2019.12.015

Cited by 6 publications

(3 citation statements)

References 29 publications

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“…When the placental trophoblast cells undergo excessive apoptosis, a large amount of harmful substances are released into the maternal circulation, resulting in the overactivation of the maternal inflammatory response system 26 . Studies have shown that the downregulated miR‐146a promotes the polarization of macrophages to M1 type, 27 thereby producing pro‐inflammatory cytokines, 28,29 while the activated TGF‐β/Smad4 pathway can increase TNF‐ α, IL‐1β, and IL‐6 levels 30 .…”

Section: Discussionmentioning

confidence: 99%

“…During normal are released into the maternal circulation, resulting in the overactivation of the maternal inflammatory response system. 26 Studies have shown that the downregulated miR-146a promotes the polarization of macrophages to M1 type, 27 thereby producing proinflammatory cytokines, 28,29 while the activated TGFβ/Smad4 pathway can increase TNF-α, IL-1β, and IL-6 levels. 30 At the same time, studies have confirmed that miR-146a can play a negative regulatory role in inflammation.…”

Section: Discussionmentioning

confidence: 99%

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Expression and role of miR‐146a and SMAD4 in placental tissue of pregnant women with preeclampsia

Cui

Liu

et al. 2022

J of Obstet and Gynaecol

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Introduction: To investigate the expression of miR-146a in severe preeclampsia (PE) and its effect on trophoblast cell proliferation, invasion and apoptosis, as well as its relationship with SMAD4. Material and Methods: Participants were divided into the severe PE group (n = 30) and the normal group (n = 30). The expression of miR-146a and SMAD4 in placenta tissue was detected by immunohistochemistry, qRT-PCR, and western blot. Trophoblast cell lines HTR-8/SVneo were cultured to detect the expression of miR-146a under the Cobalt chloride (CoCl 2 )-simulated hypoxia. The effects of miR-146a transfection on cell proliferation, invasion, apoptosis, and SMAD4 expression were analyzed. Results: Compared with the normal group, miR-146a expression was decreased and the protein and mRNA levels of SMAD4 were increased in placenta tissues of the severe PE group. Our in vitro experiments showed that the expression of miR-146a decreased after CoCl 2 treatment. Silencing miR-146a caused increased expression of SMAD4 and decreased expression of VEGF. After transfection with miR-146a inhibitor, compared with the NC group, the invasion and proliferation of HTR-8/Svneo cells were decreased, while the apoptosis was enhanced. Conclusion:The expression of miR-146a decreased in severe PE and was negatively correlated with SMAD4 expression. The expression of miR-146a was inhibited under hypoxia, and the low expression of miR-146a affected the proliferation, invasion, and apoptosis of trophoblast cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression and role of miR‐146a and SMAD4 in placental tissue of pregnant women with preeclampsia

Cui

Liu

et al. 2022

J of Obstet and Gynaecol

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“…TRAF6 is a signal transducer in the TLR4/MyD88 pathway involved in the regulation of the immune response [145,146] but also implicated in different cellular processes including regulation of proliferation, migration and invasion of cancer cells [146]. ACKR2, a chemokine scavenger, is involved in the maintenance of balance between pro and anti-inflammatory cytokines at the feto-maternal interface [147] and dysregulation of this molecule is associated with different pregnancy complications [148,149]. Wnt/β-catenin signaling pathway was also found to be affected by miR-146a-5p through direct regulation of Wnt2 expression [135].…”

Section: Non-coding Rnas-emerging Players In Oaps Pathophysiologymentioning

confidence: 99%

Trophoblast Cell Function in the Antiphospholipid Syndrome

Vrzić Petronijević,

Vilotić,

Bojić-Trbojević

et al. 2023

Biomedicines

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Antiphospholipid syndrome (APS) is a complex thrombo-inflammatory autoimmune disease characterized by the presence of antiphospholipid antibodies (aPL). Women with APS are at high risk of recurrent early pregnancy loss as well as late obstetrical complications—premature birth due to placental insufficiency or severe preeclampsia. Accumulating evidence implies that vascular thrombosis is not the only pathogenic mechanism in obstetric APS, and that the direct negative effect of aPL on the placental cells, trophoblast, plays a major role. In this review, we summarize the current findings regarding the potential mechanisms involved in aPL-induced trophoblast dysfunction. Introduction on the APS and aPL is followed by an overview of the effects of aPL on trophoblast—survival, cell function and aPL internalization. Finally, the implication of several non-coding RNAs in pathogenesis of obstetric APS is discussed, with special emphasis of their possible role in trophoblast dysfunction and the associated mechanisms.

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Histone Deacetylase Sirtuin 2 Enhances Viability of Trophoblasts Through p65-Mediated MicroRNA-146a/ACKR2 Axis

Fan

2021

Reprod. Sci.

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Expression of ACKR2 in placentas from different types of preeclampsia

Cited by 6 publications

References 29 publications

Expression and role of miR‐146a and SMAD4 in placental tissue of pregnant women with preeclampsia

Expression and role of miR‐146a and SMAD4 in placental tissue of pregnant women with preeclampsia

Trophoblast Cell Function in the Antiphospholipid Syndrome

Histone Deacetylase Sirtuin 2 Enhances Viability of Trophoblasts Through p65-Mediated MicroRNA-146a/ACKR2 Axis

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