MicroRNA-155 is involved in the remodelling of human-trophoblast-derived HTR-8/SVneo cells induced by lipopolysaccharides

Dai, Yuan; Diao, Zongli; Sun, Haixiang; Li, Ruotian; Qiu, Zhihua; Hu, Yali

doi:10.1093/humrep/der118

Cited by 68 publications

(57 citation statements)

References 40 publications

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“…Our previous work has demonstrated that the promoter of B-cell intergration cluster/miR-155 gene contains activator protein 1 and NF-κB binding motifs, and these 2 transcription factors contribute to LPS-induced expression of miR-155. 13 Here, we also showed that inhibitors of activator protein 1 and NF-κB significantly inhibited TNFα-induced upregulation of miR-155 in HUVECs. More importantly, we found that pretreatment of miR-155 inhibitor reversed TNFα-induced downregulation of eNOS expression, reduction of NO production in HUVECs, and impairment of Ach-induced endothelium-dependent vasorelaxation in human internal mammary arteries, suggesting that upregulation of miR-155 underlies, at least in part, the inhibitory effect of TNFα on eNOS expression.…”

Section: Discussionsupporting

confidence: 57%

“…13 Here, we also found that TNFα-induced upregulation of miR-155 was partially blocked by SP600125 (a c-Jun N-terminal kinase inhibitor), pyrrolidine dithiocarbamate (a NF-κB inhibitor), or the combination of both inhibitors ( Figure 3B), indicating that activator protein 1 and NF-κB are critical for TNFα-induced miR-155 production.…”

Section: Tnfα Increased Mir-155 Expression In Huvecssupporting

confidence: 54%

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Essential Role of MicroRNA-155 in Regulating Endothelium-Dependent Vasorelaxation by Targeting Endothelial Nitric Oxide Synthase

Sun¹,

Zeng²,

Li³

et al. 2012

Hypertension

292

229

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Abstract-Nitric oxide generated by endothelial nitric oxide synthase (eNOS) plays an important role in maintaining cardiovascular homeostasis. Under various pathological conditions, abnormal expression of eNOS contributes to endothelial dysfunction and the development of cardiovascular diseases. A variety of pathological stimuli has been reported to decrease eNOS expression mainly through decreasing eNOS mRNA stability by regulating the binding of several cytosolic proteins to the cis-acting sequences within eNOS mRNA 3′ untranslated regions. However, the detailed mechanisms remain elusive. Because microRNAs inhibit gene expression through binding to the 3′ untranslated regions of their target mRNAs, microRNAs may be the important posttranscriptional modulators of eNOS expression. Here, we provided evidence that eNOS is a direct target of miR-155. Overexpression of miR-155 decreased, whereas inhibition of miR-155 increased, eNOS expression and NO production in human umbilical vein endothelial cells and acetylcholineinduced endothelium-dependent vasorelaxation in human internal mammary arteries. Inflammatory cytokines including tumor necrosis factor-α increased miR-155 expression. Inhibition of miR-155 reversed tumor necrosis factor-α-induced downregulation of eNOS expression and impairment of endothelium-dependent vasorelaxation. Moreover, we observed that simvastatin attenuated tumor necrosis factor-α-induced upregulation of miR-155 and ameliorated the effects of tumor necrosis factor-α on eNOS expression and endothelium-dependent vasodilation. Simvastatin decreased miR-155 expression through interfering mevalonate-geranylgeranyl-pyrophosphate-RhoA signaling pathway. These findings indicated that miR-155 is an essential regulator of eNOS expression and endothelium-dependent vasorelaxation.Inhibition of miR-155 may be a new therapeutic approach to improve endothelial dysfunction during the development of cardiovascular diseases.

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Section: Discussionsupporting

confidence: 57%

Section: Tnfα Increased Mir-155 Expression In Huvecssupporting

confidence: 54%

Essential Role of MicroRNA-155 in Regulating Endothelium-Dependent Vasorelaxation by Targeting Endothelial Nitric Oxide Synthase

Sun¹,

Zeng²,

Li³

et al. 2012

Hypertension

292

229

View full text Add to dashboard Cite

show abstract

“…Conversely, we and others (30,31) have repeatedly shown LPS can drive induction of the pri-155 promoter in a dose-dependent manner. Our data are additionally supported by chromatin immunoprecipitation and oligonucleotide pulldown assays displaying increased binding of Ets2 to the pri-155 promoter in the presence of LPS, Ets2…”

Section: Discussionmentioning

confidence: 60%

The Role of Ets2 Transcription Factor in the Induction of MicroRNA-155 (miR-155) by Lipopolysaccharide and Its Targeting by Interleukin-10

Quinn

Mangan

Caffrey

et al. 2014

Journal of Biological Chemistry

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Background: miR-155 is strongly induced by LPS, a response inhibited by IL-10. Results: The Ets2 transcription factor is required for induction of miR-155 by LPS. IL-10 can subsequently decrease miR-155 via suppression of Ets2. Conclusion: Ets2 is an important transcription factor for regulation of miR-155. Significance: This study reports a detailed mechanism of induction of miR-155 and provides a new means of inhibition for IL-10 via suppression of Ets2.

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“…These transcription factors are implicated in trophoblast cell proliferation and differentiation, as well as pregnancy complications, such as PE [107]. Recently, an AP-1 site along with NFκB binding sites, has been identified in the miR-155 promoter [108]. Treatment of HTR8/SVneo cells with lipopolysaccharides (LPS) resulted in an increase in miR-155 levels.…”

Section: Expression Of Mirnas In Human Placentamentioning

confidence: 99%

MicroRNAs in Human Placental Development and Pregnancy Complications

Brkić

Hayder

et al. 2013

IJMS

239

174

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MicroRNAs (miRNAs) are small non-coding RNAs, which function as critical posttranscriptional regulators of gene expression by promoting mRNA degradation and translational inhibition. Placenta expresses many ubiquitous as well as specific miRNAs. These miRNAs regulate trophoblast cell differentiation, proliferation, apoptosis, invasion/migration, and angiogenesis, suggesting that miRNAs play important roles during placental development. Aberrant miRNAs expression has been linked to pregnancy complications, such as preeclampsia. Recent research of placental miRNAs focuses on identifying placental miRNA species, examining differential expression of miRNAs between placentas from normal and compromised pregnancies, and uncovering the function of miRNAs in the placenta. More studies are required to further understand the functional significance of miRNAs in placental development and to explore the possibility of using miRNAs as biomarkers and therapeutic targets for pregnancy-related disorders. In this paper, we reviewed the current knowledge about the expression and function of miRNAs in placental development, and propose future directions for miRNA studies.

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MicroRNA-155 is involved in the remodelling of human-trophoblast-derived HTR-8/SVneo cells induced by lipopolysaccharides

Abstract: LPS may induce remodelling of the human-trophoblast-derived HTR-8/SVneo cells by increasing miR-155, acting in part through the AP-1 and NF-κB pathways.

Cited by 68 publications

References 40 publications

Essential Role of MicroRNA-155 in Regulating Endothelium-Dependent Vasorelaxation by Targeting Endothelial Nitric Oxide Synthase

Essential Role of MicroRNA-155 in Regulating Endothelium-Dependent Vasorelaxation by Targeting Endothelial Nitric Oxide Synthase

The Role of Ets2 Transcription Factor in the Induction of MicroRNA-155 (miR-155) by Lipopolysaccharide and Its Targeting by Interleukin-10

MicroRNAs in Human Placental Development and Pregnancy Complications

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