Regulation and mechanism of mouse miR-130a/b in metabolism-related inflammation

Zheng, Hailiang; Dong, Xiaomin; Liu, Na; Xia, Wenmin; Zhou, Lulu; Chen, Xiaojun; Zhou, Yang; Chen, Xiao

doi:10.1016/j.biocel.2016.02.021

Cited by 28 publications

(30 citation statements)

References 29 publications

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“…miR-130a is located at chromosome 11q12, close to the 11q13 area (11). miR-130a has been found to be involved in multiple types of human diseases, including gastric (12), cervical cancer (13), chronic myeloid leukemia (14) and metabolism-related inflammation (15). Besides, reports indicate that miR-130a Epigenetic silencing of miR-130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling promote the proliferation, migration and tube formation of vascular endothelial cells (16).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic silencing of miR-130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling

Gao

Wang

Liu

et al. 2017

International Journal of Oncology

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Hemangiomas are the most common vascular tumors that occur frequently in prematures and females. microRNA (miR)-130a is associated with the growth and invasion in many tumors, and its role in hemangiomas has not been addressed so far. The present study revealed that miR‑130a was overexpressed in infantile hemangioma tissues compared with matched tumor-adjacent tissues. The inhibitor of miR-130a restrained cell growth and induced cell apoptosis in vitro. miR‑130a inhibitor also induced a cell cycle arrest at G2/M phase. Further studies revealed that tissue factor pathway inhibitor 2 (TFPI2) was a novel miR-130a target, due to miR-130a bound directly to its 3'-untranslated region and miR-130a inhibitor enhanced the expression of TFPI2. Contrary to the effects of miR-130a inhibitor, TFPI2 siRNA strongly promoted cell growth and colony formation, whereas TFPI2 overexpression contributed to the suppressing effect of miR-130a inhibitor in cell viability. Furthermore, miR-130a inhibitor reduced the activation of focal adhesion kinase (FAK)/phosphoinositide 3-kinase (PI3K)/Rac1/anti-mouse double minute (mdm2) pathway proteins, inhibited the expression and nuclear translocation of mdm2. Moreover, FAK overexpression prevented miR-130a inhibitor-induced cell cycle arrest and decrease of cell viability. In vivo experiments, miR-130a inhibition effectively suppressed the tumor growth, restrained angiogenesis by decreasing the expression of angiogenesis markers and the percentage of CD31+ and CD34+. Taken together, our research indicated that miR-130a functions as an oncogene by targeting TFPI2, miR-130a inhibition reduced the growth and angiogenesis of hemangioma by inactivating the FAK/PI3K/Rac1/mdm2 pathway. Thus, miR-130a may serve as a potential therapeutic strategy for the treatment of hemangioma.

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Section: Introductionmentioning

confidence: 99%

Epigenetic silencing of miR-130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling

Gao

Wang

Liu

et al. 2017

International Journal of Oncology

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“…miRNAs 130b-3p, 27b, and 140, which were each elevated on our PCR array during sepsis, have all been shown to regulate inflammation, specifically via NF-jB [21][22][23]26]. After determining which inflammatory miRNAs had a propensity to become elevated in the blood during sepsis, we then reviewed the literature to decide which miRNAs to continue studying for their potential interaction with eCIRP.…”

Section: Discussionmentioning

confidence: 99%

“…Their effects are mainly executed inside the cells, still leaving the question of their roles in the extracellular spaces. Its effects have been linked to the NF-jB pathway in hepatocytes [23]. Most importantly, serum levels of miRNA 130b-3p can be measured and followed [28,29,31,32].…”

Section: Discussionmentioning

confidence: 99%

“…The cycle threshold (CT) values of serum miRNAs of sham and CLP mice are presented in Fig EV1. Caenorhabditis elegans miRNA 39-3p was spiked in and used to normalize comparative CT values (Table EV1). inflammation [21][22][23], were markedly upregulated in the serum of septic mice (Fig 1A). B-D Validation of increased circulating (B) miRNA 130b-3p (n = 8 mice/group), (C) miRNA 27b (n = 8 mice/group), and (D) miRNA 140 (n = 8 mice/group).…”

Section: Sepsis Increases Serum Levels Of Mirna 130b-3pmentioning

confidence: 94%

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Extracellular microRNA 130b‐3p inhibits eCIRP‐induced inflammation

et al. 2019

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Although microRNAs regulate mRNA expression intracellularly, they are often released into the circulation in inflammatory diseases. During sepsis, secreted extracellular cold-inducible RNAbinding protein (eCIRP) acts as a damage-associated molecular pattern (DAMP), inducing tissue damage by elevating inflammatory cytokines and chemokines. Here, we report that the circulating microRNA 130b-3p inhibits eCIRP-mediated sterile and cecal ligation and puncture (CLP)-induced non-sterile inflammation. We find that levels of miR-130b-3p are increased in the serum of septic mice and patients and that it strongly interacts with recombinant murine (rm) CIRP in vitro and with eCIRP in the serum of septic mice in vivo. Combining a miR-130b-3p mimic with rmCIRP significantly decreases TNF-a release by macrophages compared to only rmCIRP-treated cells. This combined treatment also dose-dependently decreases the affinity of rmCIRP with its receptor TLR4/ MD2. Finally, injection of a miR-130b-3p mimic significantly reduces rmCIRP-or CLP-induced systemic inflammation and acute lung injury in mice. These data show that extracellular miR-130b-3p functions as a novel endogenous inhibitor of eCIRP and point to an innovative therapeutic approach to treat inflammatory diseases.

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“…An increasing number of studies have shown that transcription factors are capable of binding to miRNA promoter elements and modulating miRNA transcription [ 38 , 39 , 40 ]. Therefore, we analyzed the transcriptional mechanism of miR-25-3p in this study.…”

Section: Discussionmentioning

confidence: 99%

miR-25-3p, Positively Regulated by Transcription Factor AP-2α, Regulates the Metabolism of C2C12 Cells by Targeting Akt1

Zhang

Chen

Tao

et al. 2018

IJMS

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miR-25, a member of the miR-106b-25 cluster, has been reported as playing an important role in many biological processes by numerous studies, while the role of miR-25 in metabolism and its transcriptional regulation mechanism remain unclear. In this study, gain-of-function and loss-of-function assays demonstrated that miR-25-3p positively regulated the metabolism of C2C12 cells by attenuating phosphoinositide 3-kinase (PI3K) gene expression and triglyceride (TG) content, and enhancing the content of adenosine triphosphate (ATP) and reactive oxygen species (ROS). Furthermore, the results from bioinformatics analysis, dual luciferase assay, site-directed mutagenesis, qRT-PCR, and Western blotting demonstrated that miR-25-3p directly targeted the AKT serine/threonine kinase 1 (Akt1) 3′ untranslated region (3′UTR). The core promoter of miR-25-3p was identified, and the transcription factor activator protein-2α (AP-2α) significantly increased the expression of mature miR-25-3p by binding to its core promoter in vivo, as indicated by the chromatin immunoprecipitation (ChIP) assay, and AP-2α binding also downregulated the expression of Akt1. Taken together, our findings suggest that miR-25-3p, positively regulated by the transcription factor AP-2α, enhances C2C12 cell metabolism by targeting the Akt1 gene.

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Regulation and mechanism of mouse miR-130a/b in metabolism-related inflammation

Cited by 28 publications

References 29 publications

Epigenetic silencing of miR-130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling

Epigenetic silencing of miR-130a ameliorates hemangioma by targeting tissue factor pathway inhibitor 2 through FAK/PI3K/Rac1/mdm2 signaling

Extracellular microRNA 130b‐3p inhibits eCIRP‐induced inflammation

miR-25-3p, Positively Regulated by Transcription Factor AP-2α, Regulates the Metabolism of C2C12 Cells by Targeting Akt1

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