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Identification of microRNAs involved in NOD-dependent induction of pro-inflammatory genes in pulmonary endothelial cells

ABSTRACT: Identification of microRNAs involved in NOD-dependent induction of pro-inflammatory genes in pulmonary endothelial cells

PROVIDER: PRJNA608273 | ENA |

REPOSITORIES: ENA

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Identification of microRNAs involved in NOD-dependent induction of pro-inflammatory genes in pulmonary endothelial cells.

Project description:The nucleotide-binding oligomerization domain-containing proteins (NOD) 1 and 2 are mammalian cytosolic pattern recognition receptors sensing bacterial peptidoglycan fragments in order to initiate cytokine expression and pathogen host defense. Since endothelial cells are relevant cells for pathogen recognition at the blood/tissue interface, we here analyzed the role of NOD1- and NOD2-dependently expressed microRNAs (miRNAs, miR) for cytokine regulation in murine pulmonary endothelial cells. The induction of inflammatory cytokines in response to NOD1 and NOD2 was confirmed by increased expression of tumour necrosis factor (Tnf)-α and interleukin (Il)-6. MiRNA expression profiling revealed NOD1- and NOD2-dependently regulated miRNA candidates, of which miR-147-3p, miR-200a-3p, and miR-298-5p were subsequently validated in pulmonary endothelial cells isolated from Nod1/2-deficient mice. Analysis of the two down-regulated candidates miR-147-3p and miR-298-5p revealed predicted binding sites in the 3' untranslated region (UTR) of the murine Tnf-α and Il-6 mRNA. Consequently, transfection of endothelial cells with miRNA mimics decreased Tnf-α and Il-6 mRNA levels. Finally, a novel direct interaction of miR-298-5p with the 3' UTR of the Il-6 mRNA was uncovered by luciferase reporter assays. We here identified a mechanism of miRNA-down-regulation by NOD stimulation thereby enabling the induction of inflammatory gene expression in endothelial cells.

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Identification of microRNAs involved in NOD-dependent induction of pro-inflammatory genes in pulmonary endothelial cells

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Project description:Pulmonary arterial hypertension (PAH) is a vascular remodeling disease characterized by enhanced pulmonary artery smooth muscle cell (PASMC) proliferation and suppressed apoptosis. Downregulation of the BMPR2 gene along with activation of the transcription factor NFAT have been implicated in the maintenance of pro-proliferative and anti-apoptotic stages of cells. Since an increasing number of microRNAs have been implicated in the regulation of genes specifically important for cell proliferation and apoptosis, we hypothesized that microRNAs might be associated with these cellular features in the etiology of PAH. We demonstrate that downregulation of one such microRNA (miR-204) in human PAH-PASMC promotes the activation of an Src/STAT3/NFAT axis that increases PAH-PASMC proliferation and their resistance to apoptosis. Stimulation experiments using the pro-PAH factors (PDGF, endothelin-1 and angiotensin II) and time course analysis in experimental PAH show that STAT3 activation leads to miR-204 downregulation, thereby activating an Src-dependent positive feedback loop sustaining STAT3 and activating NFAT. More importantly, restoring miR-204 expression decreases proliferation and resistance to apoptosis in human and in an experimental PAH model. Taken together, our study uncovers a new STAT3-miR-204-Src/STAT3/NFAT axis that links the STAT3-dependent downregulation of BMPR2 with the NFAT-mediated pro-proliferative and anti-apoptotic phenotype observed in PAH. Our data point toward a novel potential strategy for treating patients with PAH. Comparative expression profiling of PAH versus healthy patients to evaluate the modulated genes in the disease. Following the demonstration of the downregulation of miR-204 in PAH we want to investigate the effect of the inhibition (using antagomir) of miR-204 expression in PASMC cells.

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