Up regulation of miR-96-5p is responsible for TiO2 NPs induced invasion dysfunction of human trophoblastic cells via disturbing Ezrin mediated cytoskeletons arrangement

Mao, Zhilei; Guan, Yusheng; Li, Ting; Zhang, Lina; Liu, Menglu; Xing, Baoling; Yao, Mengmeng; Chen, Minjian

doi:10.1016/j.biopha.2019.109125

Cited by 8 publications

(7 citation statements)

References 35 publications

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“…Accumulation in the placenta may also lead to placental dysfunction (e.g., dysregulation of vascularization, inhibition of cell proliferation, induction of apoptosis) and subsequent foetal growth restriction [11]. In addition to the findings in these rodent studies, TiO 2 -NPs can trigger autophagy and mitochondrial dysfunction in vitro in human trophoblast cells [65,66], and further impair the cell migration [67] that is needed for trophoblastic invasion in the uterine wall, permitting embryo implantation. Therefore, additional studies are needed to quantify and further characterize the human foetal exposure to TiO 2 -NPs shown in our study, together with studies in animals chronically exposed to TiO 2 during pregnancy, including from the oral route, to determine the potential hazards for foetal development and newborn health.…”

Section: Discussionmentioning

confidence: 77%

Basal Ti level in the human placenta and meconium and evidence of a materno-foetal transfer of food-grade TiO2 nanoparticles in an ex vivo placental perfusion model

et al. 2020

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Background Titanium dioxide (TiO2) is broadly used in common consumer goods, including as a food additive (E171 in Europe) for colouring and opacifying properties. The E171 additive contains TiO2 nanoparticles (NPs), part of them being absorbed in the intestine and accumulated in several systemic organs. Exposure to TiO2-NPs in rodents during pregnancy resulted in alteration of placental functions and a materno-foetal transfer of NPs, both with toxic effects on the foetus. However, no human data are available for pregnant women exposed to food-grade TiO2-NPs and their potential transfer to the foetus. In this study, human placentae collected at term from normal pregnancies and meconium (the first stool of newborns) from unpaired mothers/children were analysed using inductively coupled plasma mass spectrometry (ICP-MS) and scanning transmission electron microscopy (STEM) coupled to energy-dispersive X-ray (EDX) spectroscopy for their titanium (Ti) contents and for analysis of TiO2 particle deposition, respectively. Using an ex vivo placenta perfusion model, we also assessed the transplacental passage of food-grade TiO2 particles. Results By ICP-MS analysis, we evidenced the presence of Ti in all placentae (basal level ranging from 0.01 to 0.48 mg/kg of tissue) and in 50% of the meconium samples (0.02–1.50 mg/kg), suggesting a materno-foetal passage of Ti. STEM-EDX observation of the placental tissues confirmed the presence of TiO2-NPs in addition to iron (Fe), tin (Sn), aluminium (Al) and silicon (Si) as mixed or isolated particle deposits. TiO2 particles, as well as Si, Al, Fe and zinc (Zn) particles were also recovered in the meconium. In placenta perfusion experiments, confocal imaging and SEM-EDX analysis of foetal exudate confirmed a low transfer of food-grade TiO2 particles to the foetal side, which was barely quantifiable by ICP-MS. Diameter measurements showed that 70 to 100% of the TiO2 particles recovered in the foetal exudate were nanosized. Conclusions Altogether, these results show a materno-foetal transfer of TiO2 particles during pregnancy, with food-grade TiO2 as a potential source for foetal exposure to NPs. These data emphasize the need for risk assessment of chronic exposure to TiO2-NPs during pregnancy.

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Section: Discussionmentioning

confidence: 77%

Basal Ti level in the human placenta and meconium and evidence of a materno-foetal transfer of food-grade TiO2 nanoparticles in an ex vivo placental perfusion model

et al. 2020

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“…Our study revealed that circCTNNB1 acted as an miR-96-5p sponge to regulate astrocyte survival. MiR-96-5p plays pleiotropic roles in cancer [ 43 ], wound healing [ 44 ], placental dysfunction [ 45 ] and hepatic steatosis [ 46 ]. Consistent with prior results, the miR-96-5p expression level was elevated following cerebral ischemia [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

CircRNA CTNNB1 (circCTNNB1) ameliorates cerebral ischemia/reperfusion injury by sponging miR-96-5p to up-regulate scavenger receptor class B type 1 (SRB1) expression

et al. 2022

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Emerging studies show that circRNA catenin beta 1 (circCTNNB1) plays a critical role in cancer. However, the expression and function of circCTNNB1 in cerebral ischemia/reperfusion injury (IRI) have not been reported. The present study discovered that circCTNNB1 and scavenger receptor class B type 1 (SRB1) expression levels were significantly down-regulated in mouse astrocytes (mAS) treated with oxygen glucose deprivation and reperfusion (OGD/R), and similar results were observed in a mouse middle cerebral artery occlusion model. Overexpression of circCTNNB1 alleviated cell apoptosis, oxidative stress and the inflammatory response induced by OGD/R in vitro . Up-regulation of circCTNNB1 increased SRB1 expression levels to protect mAS cells from OGD/R-induced damage. CircCTNNB1 and SRB1 interacted with miR-96-5p, and the overexpression of miR-96-5p efficiently reversed the function of circCTNNB1 in OGD/R-treated mAS cells. CircCTNNB1 protected against cerebral ischemia-reperfusion injury by up-regulating SRB1 in vivo . In conclusion, our findings suggest that circCTNNB1 acts as a competitive endogenous RNA for miR-96-5p to alleviate cerebral IRI, which provides novel evidence that circCTNNB1 and SRB1 may be biomarkers and therapeutic targets for cerebral IRI.

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“…Targetscan software has predicted the binding sequences between NAMPT and miR-96-5p. In order to confirm the relationship between NAMPT and miR-96-5p, dual luciferase reporter assay was performed as previously described [ 14 ]. The fragment of NAMPT 3′-UTR (NAMPT-WT) containing the predicted binding sites of miR-96-5p and its mutant (NAMPT-MUT) sequences were cloned into the downstream of the luciferase gene in pGL-control reporter plasmid vector (Promega, Madison, WI, U.S.A.), separately.…”

Section: Methodsmentioning

confidence: 99%

MiR-96-5p alleviates inflammatory responses by targeting NAMPT and regulating the NF-κB pathway in neonatal sepsis

Chen

et al. 2020

Bioscience Reports

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Abstract Neonatal septicemia is a serious infectious disease in the neonatal period. MicroRNAs (miRNAs) have been reported to participate in the inflammatory responses in neonatal sepsis. The aim of the present study was to explore the effects and molecular mechanism of miR-96-5p on regulating the inflammatory responses in neonatal sepsis. MiR-96-5p was low expressed while nicotinamide phosphoribosyltransferase (NAMPT) was high expressed in the serum of neonatal septicemia patients. The expression of miR-96-5p was decreased in LPS-induced inflammatory responses. Besides, miR-95-5p relieved LPS-induced inflammatory responses in RAW264.7 cells. NAMPT was demonstrated as a potential target of miR-96-5p, and knockdown of NAMPT reduced inflammatory in RAW264.7 cells stimulated with LPS. Moreover, overexpression of NAMPT reversed the effects of miR-96-5p on LPS-induced inflammatory responses. In addition, miR-96-5p inhibited nuclear factor (NF)-κB signaling pathway in RAW264.7 cells stimulated with LPS. MiR-96-5p alleviated inflammatory responses via targeting NAMPT and inhibiting NF-κB pathway in neonatal sepsis.

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Up regulation of miR-96-5p is responsible for TiO2 NPs induced invasion dysfunction of human trophoblastic cells via disturbing Ezrin mediated cytoskeletons arrangement

Cited by 8 publications

References 35 publications

Basal Ti level in the human placenta and meconium and evidence of a materno-foetal transfer of food-grade TiO2 nanoparticles in an ex vivo placental perfusion model

Basal Ti level in the human placenta and meconium and evidence of a materno-foetal transfer of food-grade TiO2 nanoparticles in an ex vivo placental perfusion model

CircRNA CTNNB1 (circCTNNB1) ameliorates cerebral ischemia/reperfusion injury by sponging miR-96-5p to up-regulate scavenger receptor class B type 1 (SRB1) expression

MiR-96-5p alleviates inflammatory responses by targeting NAMPT and regulating the NF-κB pathway in neonatal sepsis

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