MicroRNA-155 Regulates Inflammatory Cytokine Production in Tumor-associated Macrophages via Targeting C/EBPβ

He, Min; Xu, Zhihao; Ding, Tao; Kuang, Dong-Ming; Zheng, Limin

doi:10.1038/cmi.2009.45

Cited by 174 publications

(147 citation statements)

References 44 publications

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“…All steps of the luciferase reporter assay were performed as previously described (15,22). NIH-3T3 cells were seeded at 3x10 4 cells/well in 48-well plates and co-transfected with 400 ng of pRNAT-cMV32-cgFP-mir182 or pRNAT-cMV32-cgFP or pRNAT-cMV32-cgFP-mir182-Mut, 20 ng of pgL3cm-cTTN-3UTR-WT or pgL3cm-cTTN-3UTR-Mut, and pRL-TK (Promega, Madison, USA) using the Lipofectamine 2000 reagent according to the manufacturer's protocol.…”

Section: Flow Cytometric (Fcm) Analysis Of Cell Cycle By Propidium Iomentioning

confidence: 99%

microRNA-182 inhibits the proliferation and invasion of human lung adenocarcinoma cells through its effect on human cortical actin-associated protein

Zhang

Liu

Huang³

et al. 2011

Int J Mol Med

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Abstract. Lung cancer is one of the main causes of cancer death worldwide. The cortactin gene, CTTN, may play a pivotal role in the proliferation and invasion of tumors. A microRNA (miR-182) was cloned and used to study the expression of CTTN and its regulatory effects on the proliferation and invasion of the lung cancer cell line, A549. cortactin protein and CTTN mRNA expression decreased in A549 cells that were transfected with the miR-182 expression plasmid. A cell proliferation assay indicated that miR-182 expression affected cell cycle regulation and suppressed proliferation of lung cancer cells in vitro. In addition, xenograft experiments confirmed the suppression of tumor growth in vivo, which was due to the promotion of apoptosis. In conclusion, endogenous mature miR-182 expression may have an important role in the pathogenesis of lung cancer through its interference with the target gene CTTN by epigenetic modification.

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Section: Flow Cytometric (Fcm) Analysis Of Cell Cycle By Propidium Iomentioning

confidence: 99%

microRNA-182 inhibits the proliferation and invasion of human lung adenocarcinoma cells through its effect on human cortical actin-associated protein

Zhang

Liu

Huang³

et al. 2011

Int J Mol Med

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“…Depletion of the Akt2 isoform in peritoneal macrophages abrogates M1 activation and promotes M2 phenotype by inducing C/EBPb (22,25), a transcriptional regulator of Arg-1 expression (30). Akt2 depletion induces C/EBPb via negative regulation of the microRNA (miRNA) miR-155, known to target C/EBPb and promote M1 (22,25,31). Additionally, TLR4 signaling was shown to play an important role in alveolar macrophage activation in animal models of ALI (12,32,33).…”

mentioning

confidence: 99%

Akt2 Deficiency Protects from Acute Lung Injury via Alternative Macrophage Activation and miR-146a Induction in Mice

Vergadi

Vaporidi

Theodorakis

et al. 2014

The Journal of Immunology

142

103

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Acute respiratory distress syndrome (ARDS) is a major cause of respiratory failure, with limited effective treatments available. Alveolar macrophages participate in the pathogenesis of ARDS. To investigate the role of macrophage activation in aseptic lung injury and identify molecular mediators with therapeutic potential, lung injury was induced in wild-type (WT) and Akt2−/− mice by hydrochloric acid aspiration. Acid-induced lung injury in WT mice was characterized by decreased lung compliance and increased protein and cytokine concentration in bronchoalveolar lavage fluid. Alveolar macrophages acquired a classical activation (M1) phenotype. Acid-induced lung injury was less severe in Akt2−/− mice compared with WT mice. Alveolar macrophages from acid-injured Akt2−/− mice demonstrated the alternative activation phenotype (M2). Although M2 polarization suppressed aseptic lung injury, it resulted in increased lung bacterial load when Akt2−/− mice were infected with Pseudomonas aeruginosa. miR-146a, an anti-inflammatory microRNA targeting TLR4 signaling, was induced during the late phase of lung injury in WT mice, whereas it was increased early in Akt2−/− mice. Indeed, miR-146a overexpression in WT macrophages suppressed LPS-induced inducible NO synthase (iNOS) and promoted M2 polarization, whereas miR-146a inhibition in Akt2−/− macrophages restored iNOS expression. Furthermore, miR-146a delivery or Akt2 silencing in WT mice exposed to acid resulted in suppression of iNOS in alveolar macrophages. In conclusion, Akt2 suppression and miR-146a induction promote the M2 macrophage phenotype, resulting in amelioration of acid-induced lung injury. In vivo modulation of macrophage phenotype through Akt2 or miR-146a could provide a potential therapeutic approach for aseptic ARDS; however, it may be deleterious in septic ARDS because of impaired bacterial clearance.

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“…All the steps were performed as previously described (35,36). NIH-3T3 cells were seeded at 3x10 4 /well in 48-well plates and co-transfected with 400 ng of pRNAT-cMV32-cgFP-mir155 or pRNAT-cMV32-cgFP or pRNAT-cMV32-cgFP-mir155-Mut, 20 ng of pgL3cm-AT1R-3UTR-WT or pgL3cm-AT1R-3UTR-Mut, and pRL-TK (Promega, Madison, USA) using the Lipofectamine 2000 Reagent according to the manufacturer's protocol.…”

Section: Rna Extraction and Analysis By Quantitative Real-time Pcr (Qmentioning

confidence: 99%

microRNA-155 regulates angiotensin II type 1 receptor expression in umbilical vein endothelial cells from severely pre-eclamptic pregnant women

Cheng

Liu

Jiang³

et al. 2011

Int J Mol Med

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Abstract. Angiotensin II is critical in pre-eclampsia pathogenesis. In addition, microRNA-155 regulates angiotensin II type 1 receptor expression. We have explored the function of microRNA-155 in pre-eclamptic pregnant women. Human umbilical vein endothelial cells were isolated and cultured from healthy puerperant women and pre-eclampsia patients. The cells were transfected with a mature microRNA-155 plasmid. The effect of microRNA-155 was assessed by Northern blotting, in situ hybridization, quantitative real-time PCR, immunofluorescent staining and Western blotting. In addition, activation of extracellular signal-regulated kinase 1/2 was assessed by co-immunoprecipitation and Western blotting. Severely pre-eclamptic pregnant women expressed less mature miR-155 compared to healthy pregnant women. In addition, angiotensin II type 1 receptor expression decreased substantially in healthy cells and miR-155-transfected cells compared to miR-155-mutant-transfected cells and cells from pre-eclamptic patients. Mature miR-155 reduced angiotensin II-induced extracellular signal-regulated kinase 1/2 activation. In conclusion, endogenous mature miR-155 expression may be an important contributor to the pathogenesis of severe pre-eclampsia.

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MicroRNA-155 Regulates Inflammatory Cytokine Production in Tumor-associated Macrophages via Targeting C/EBPβ

Cited by 174 publications

References 44 publications

microRNA-182 inhibits the proliferation and invasion of human lung adenocarcinoma cells through its effect on human cortical actin-associated protein

microRNA-182 inhibits the proliferation and invasion of human lung adenocarcinoma cells through its effect on human cortical actin-associated protein

Akt2 Deficiency Protects from Acute Lung Injury via Alternative Macrophage Activation and miR-146a Induction in Mice

microRNA-155 regulates angiotensin II type 1 receptor expression in umbilical vein endothelial cells from severely pre-eclamptic pregnant women

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