MicroRNA-135b suppresses extravillous trophoblast-derived HTR-8/SVneo cell invasion by directly down regulating CXCL12 under low oxygen conditions

Tamaru, Shunsuke; Mizuno, Yosuke; Tochigi, Hideno; Kajihara, Takeshi; Okazaki, Yasushi; Okagaki, Ryugo; Kamei, Yoshimasa; Ishihara, Osamu; Itakura, Atsuo

doi:10.1016/j.bbrc.2015.04.055

Cited by 31 publications

(19 citation statements)

References 26 publications

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“…Primary trophoblasts secrete high levels of CXCL12 to promote their own invasiveness and matrixmetalloproteinase activity [33,34]. Several studies have reported that CXCL12 is crucial for regulating trophoblast phenotypes during the first trimester [18,35]. Our study suggested that inhibition of CXCL12 expression by nicotine is a novel regulatory system that could influence the invasiveness of HTR-8/SVneo cells.…”

Section: Discussionmentioning

confidence: 62%

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Nicotine Suppresses the Invasiveness of Human Trophoblasts by Downregulation of CXCL12 Expression through the Alpha-7 Subunit of the Nicotinic Acetylcholine Receptor

Chen

Huang

et al. 2020

Reprod. Sci.

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Smoke exposure during pregnancy has detrimental effects upon numerous fetal and neonatal outcomes. Nicotine (the main component of tobacco) has been suggested to affect placental development. During placental development, efficient invasion by trophoblasts is required for establishment of the fetus-maternal circulation. In this study we explored the regulation of trophoblast invasion by nicotine. An immortalized first trimester extravillous trophoblast cell line (HTR-8/SVneo cells) was used for all the experiments, which were treated by nicotine, methyllycaconitine, and C-X-C motif chemokine ligand 12 (CXCL12). Total RNA and protein were used to study the expressions of nicotinic acetylcholine receptors (nAChRs), and transwell assay was used to study invasiveness. Changes of RNA expression due to nicotine treatment were detected by RNA sequence. Level of CXCL12 mRNA was verified by quantitative PCR. We showed that HTR-8/SVneo expressed subunits α2-4, α7, α9, β1, and β2 of nAChRs. Nicotine downregulated CXCL12 expression and inhibited trophoblast invasion. Methyllycaconitine, as an antagonist of the α7 homopolymer, blocked the inhibitory effect of nicotine. CXCL12 could rescue the nicotine-induced inhibitory effect on invasion of HTR-8/SVneo cells. These results suggest that the α7 subunit of the nAChR has important roles in modulating trophoblast invasion through CXCL12.

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Section: Discussionmentioning

confidence: 62%

“…However, the effect of nicotine on trophoblasts has not been deeply studied. C-X-C motif chemokine ligand 12 (CXCL12) is an important chemokine on regulating trophoblast phenotypes during the first trimester [17][18][19]. Nonetheless, whether nicotine can influence trophoblast through regulating CXCL12 expression is unknown.…”

Section: Introductionmentioning

confidence: 99%

Nicotine Suppresses the Invasiveness of Human Trophoblasts by Downregulation of CXCL12 Expression through the Alpha-7 Subunit of the Nicotinic Acetylcholine Receptor

Chen

Huang

et al. 2020

Reprod. Sci.

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“…Studies showed that the expression of microRNA-135b increases hypoxic conditions, which leads to suppression of CXCL12 expression and trophoblastic invasion. [58]. microRNA-135b and microRNA-130a-3p target the 3′UTR sequence of CXCL-12 and suppress its expression.…”

Section: Resultsmentioning

confidence: 99%

“…microRNA-135b and microRNA-130a-3p target the 3′UTR sequence of CXCL-12 and suppress its expression. microRNA-130a-3p has an overexpression in nasopharyngeal carcinoma [58,59]. In addition, Pillai et al showed that miR-886-3p reduces the expression of CXCL-12 in human marrow stromal cells [60].…”

Section: Resultsmentioning

confidence: 99%

Adverse effects of nicotine on endometrium receptivity markers: and protective effect of caffeic acid phenyl ester

Namdari

MOHAMMADIAN

Khajeh

et al. 2020

Preprint

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Background nicotine adversely affects the female reproductive system and changes the methylation pattern of some genes in the placenta. In contrast, caffeic acid phenylethyl ester) CAPE (, as a potent antioxidant, has protective effects against the harmful effects of oxygen free radical molecules, methotrexate, and pesticides on the reproductive system. To find the effect of nicotine on the endometrium, we investigated three markers of endometrium receptivity including fibroblast growth factor 2, vascular endothelial growth factors A, and C-X-C motif chemokine ligand 12 and also changes in methylation levels of CXCL-12 gene promoter. In addition, we evaluated the protective effect of CAPE against nicotine. Methods the appropriate treatment dose was selected based on the literature, the endometrial stromal cells were divided into 4 groups, including control, treated with nicotine, CAPE, and nicotine followed by CAPE. Finally, the quantitative polymerase chain reaction and Methylation-Specific PCR were carried out. Results The results showed that treatment of endometrial stromal cells with nicotine (10− 6 µM) for 24 h significantly reduced expression of CXCL-12, FGF, and VEGFA genes. However, a decrease in CXCL-12 expression was not associated with increased methylation levels in the studied promoter region. In contrast, endometrial stromal cells treated with CAPE (4 µg/ml) for 24 h adverse significantly nicotine-induced reduction of CXCL-12, FGF, and VEGFA genes expression. Conclusion Exposure to nicotine has negative effects on uterine receptivity, implantation, and fertility, via reducing the expression of VEGFA, CXCL-12, and FGF2 genes. In contrast, CAPE has a protective effects and improves these genes expression.

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“…miRNA135b mediates low oxygen-induced reduction of extravillous trophoblast-derived HTR-8/SVneo cell invasion by inhibiting its target gene CXCL12, an invasion-promoting factor (Tamaru et al 2015). MicroRNA-155 inhibits migration of human HTR-8/ SVneo cell by downregulating cyclin D1 (Dai et al 2012).…”

Section: R232mentioning

confidence: 99%

Progress in the understanding of the etiology and predictability of fetal growth restriction

Tang

Liu

et al. 2017

Reproduction

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Fetal growth restriction (FGR) is defined as the failure of fetus to reach its growth potential for various reasons, leading to multiple perinatal complications and adult diseases of fetal origins. Shallow extravillous trophoblast (EVT) invasion-induced placental insufficiency and placental dysfunction are considered the main reasons for idiopathic FGR. In this review, first we discuss the major characteristics of anti-angiogenic state and the pro-inflammatory bias in FGR. We then elaborate major abnormalities in placental insufficiency at molecular levels, including the interaction between decidual leukocytes and EVT, alteration of miRNA expression and imprinted gene expression pattern in FGR. Finally, we review current animal models used in FGR, an experimental intervention based on animal models and the progress of predictive biomarker studies in FGR. Free Chinese abstract: A Chinese translation of this abstract is freely available at http://www.reproduction-online.org/content/153/6/ R227/suppl/DC1. Reproduction (2017) 153 R227-R240

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MicroRNA-135b suppresses extravillous trophoblast-derived HTR-8/SVneo cell invasion by directly down regulating CXCL12 under low oxygen conditions

Cited by 31 publications

References 26 publications

Nicotine Suppresses the Invasiveness of Human Trophoblasts by Downregulation of CXCL12 Expression through the Alpha-7 Subunit of the Nicotinic Acetylcholine Receptor

Nicotine Suppresses the Invasiveness of Human Trophoblasts by Downregulation of CXCL12 Expression through the Alpha-7 Subunit of the Nicotinic Acetylcholine Receptor

Adverse effects of nicotine on endometrium receptivity markers: and protective effect of caffeic acid phenyl ester

Progress in the understanding of the etiology and predictability of fetal growth restriction

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