Exposure to environmental bisphenol A inhibits HTR-8/SVneo cell migration and invasion

Pu, Wei; Ru, Dongqing; Li, Xiaoqian; Shi, Dongyan; Zhang, Mingshun; Xu, Qing; Zhou, Hong; Wen, Shuang

doi:10.7555/jbr.34.20200013

Cited by 13 publications

(7 citation statements)

References 35 publications

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“…Data were presented as the mean ± SD and processed using GraphPad Prism 8.0 (GraphPad Software, San Diego, USA). Data were in accordance with the normal distribution by Shapiro-Wilk test [ 27 ], and comparisons were conducted using one-way ANOVA [ 28 ] followed by Tukey’s post hoc test [ 29 ]. P < 0.05 was considered to indicate a statistically significant difference.…”

Section: Methodsmentioning

confidence: 99%

C1q/tumor necrosis factor related protein 6 (CTRP6) regulates the phenotypes of high glucose-induced gestational trophoblast cells via peroxisome proliferator-activated receptor gamma (PPARγ) signaling

Zhang

Bai

2021

Bioengineered

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Multiple studies have confirmed that adipokines are compactly relevant to insulin resistance and participate in the pathogenesis of gestational diabetes mellitus (GDM). This paper aimed to study the effects of C1q/tumor necrosis factor related protein (CTRP)6 on the phenotypes of trophoblast cells, covering cell proliferation, invasion and migration, and initially explore the mechanism. High glucose was used to induce trophoblast cells to establish an in vitro model. The expression levels of CTRP6 were firstly determined, and then the effects of CTRP6 knockdown on cell viability, apoptosis, migration and invasion were assessed using CCK8, TUNEL, wound healing, Transwell assays. Moreover, the role of peroxisome proliferator-activated receptor gamma (PPARγ), probable target of CTRP6, was evaluated through co-transfection with PPARγ overexpression vector. The results of the present study revealed that CTRP6 and PPARγ were both upregulated in high glucose-induced cells. And CTRP6 knockdown could significantly elevate the abilities of cell viability, migration and invasion, and avoid cell apoptosis. In addition, PPARγ overexpression was found to restrain the protective effects of CTRP6 knockdown on the above aspects, indicating CTRP6 played a role in trophoblast cells via inhibiting PPARγ expression. In conclusion, CTRP6 regulated the viability, migration and invasion of high glucose-induced gestational trophoblast cells through PPARγ signaling.

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Section: Methodsmentioning

confidence: 99%

C1q/tumor necrosis factor related protein 6 (CTRP6) regulates the phenotypes of high glucose-induced gestational trophoblast cells via peroxisome proliferator-activated receptor gamma (PPARγ) signaling

Zhang

Bai

2021

Bioengineered

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“…In mouse placenta, BPA causes a decrease in the labyrinthine and spongiotrophoblast zone proportions with narrowing of the intervillous spaces [ 34 , 35 , 36 , 37 ]. The exact mechanisms as to how this occurs seems to be debatable; matrix metalloproteinase-2/9 (MMP2/MMP9) seems to be involved, but upregulation or downregulation occurs depending on the model used [ 34 , 35 , 38 , 39 ].…”

Section: Resultsmentioning

confidence: 99%

Actions of Bisphenol A on Different Feto-Maternal Compartments Contributing to Preterm Birth

Vidal

Menon

et al. 2022

IJMS

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Preterm birth remains to be one of the most prevalent obstetric complications worldwide. Since there are multiple etiological factors associated with this disease process, an integrative literature search in PubMed and Scopus databases on possible mechanism of action and effect of bisphenols on exposure on human or animal placental samples in preterm birth was conducted. From 2332 articles on initial literature search, 63 studies were included for full data extraction. Altogether, several pathways were shown to be possibly affected by bisphenols, leading to dysregulations in structural and endocrine foundation in the placenta, potential induction of senescence and failure of decidualization in the decidua, and possible propagation of inflammation in the fetal membranes. Combined, these actions may eventually counteract bisphenol-induced relaxation of the myometrium and promote contractility alongside fetal membrane weakening. In totality, these individual impairments in gestation-critical processes may lead to failure of maintenance of pregnancy, and thus effecting preterm birth.

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“…Few studies about the effect of BPA on the trophoblast migration were performed [67][68][69]74], while no information is available yet on the effect of BPS on this process. Present results indicate that only BPA affected cell migration ability.…”

Section: Discussionmentioning

confidence: 99%

“…Similar to cell proliferation, also data on BPA effect on HTR8/SVneo cell migration are conflicting. Some studies [67,68,74] observed that migration and invasion were reduced following BPA exposure, while others [69] assessed that BPA enhances cell migration through ERK1/2 stimulation. The present work reports a reduction of migration at micromolar BPA concentrations.…”

Section: Discussionmentioning

confidence: 99%

Comparing effects and action mechanisms of BPA and BPS on HTR-8/SVneo placental cells

Profita

Fabbri

Spisni

et al. 2021

Biology of Reproduction

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Bisphenol A (BPA) is one of the most investigated compound as a suspected endocrine disrupting chemical. It has been found at nM concentrations in the maternal serum, cord serum, and amniotic fluid and also permeates placental tissues. Attempts are being made to replace BPA with the analog Bisphenol S (BPS). Also BPS was found in maternal and umbilical cord serum, and urine samples from a large population of pregnant women. A few studies investigated BPA impact on the placentation process, and even less are available for BPS. This work aimed to elucidate and compare the effects of BPA and BPS on physiological functions of HTR-8/SVneo cells, derived from extravillous trophoblast of first-trimester pregnancy. Proliferation and migration ability of trophoblast cells were assessed in vitro after exposure to BPA or BPS (10−13 - 10−3 M). Further, induction of the inflammatory response by the bisphenols was studied. To provide insight into the molecular pathways implicated in the responses, experiments were carried out in the presence or absence of tamoxifen as estrogen receptors (ERs) blocker, and U0126 as ERK1/2 phosphorylation inhibitor. Data indicate that BPA significantly affects both proliferation and migration of HTR-8/SVneo cells, through ER and ERK1/2 mediated processes. Differently, BPS only acts on proliferation, again through ER and ERK1/2 mediated processes. BPS, but not BPA, induces secretion of interleukins 6 and 8. Such effect is inhibited by blocking ERK1/2 phosphorylation. To the best of our knowledge, these are the first data showing that BPS affects trophoblast functions through ER/MAPK modulation.

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Exposure to environmental bisphenol A inhibits HTR-8/SVneo cell migration and invasion

Cited by 13 publications

References 35 publications

C1q/tumor necrosis factor related protein 6 (CTRP6) regulates the phenotypes of high glucose-induced gestational trophoblast cells via peroxisome proliferator-activated receptor gamma (PPARγ) signaling

C1q/tumor necrosis factor related protein 6 (CTRP6) regulates the phenotypes of high glucose-induced gestational trophoblast cells via peroxisome proliferator-activated receptor gamma (PPARγ) signaling

Actions of Bisphenol A on Different Feto-Maternal Compartments Contributing to Preterm Birth

Comparing effects and action mechanisms of BPA and BPS on HTR-8/SVneo placental cells

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